The hazards of reductionistic neuroscience interpretation: Revisiting anomalies and subjective experience linked with the brain.
Vernon M Neppe MD, PhD, FRSSAf, DFAPA, BN&NP, DPM, FRCPC, FFPsych, MMed.
Pacific Neuropsychiatric Institute, Seattle, WA, USA and
Dept of Psychiatry, St. Louis U., St Louis, MO1
Abstract
Several recent neuroscience research publications on alleged psi and their brain correlates are examined. Superficial evaluations of these studies could support the model of materialistic reductionism, namely, that specific psi experiences derive solely from brain physiology. Detailed analyses in this paper dispute this conclusion.
Five different objective or subjective psi-brain situations are evaluated:
These studies (#1-2) evaluated retrospective subjective paranormal experiences (SPEs), not psi itself, because the reports involved purely subjective experiences.
These studies all involved
attempted brain imaging of actual psi (OPE—objective paranormal experience).
Detailed
analyses of the stimulation of focal brain areas and “OBE” (in #1),
of the REM intrusion / “NDE” study (in #2) and of Moulton’s fMRI
brain study (in #3) all reveal flawed methodology and/or misinterpretations.
The author suggests two other brain models. These could highlight a more appropriate, productive approach (#4 and #5):
The approaches reflected in all five of these areas suggest that analysis of SPEs constitute a major phenomenological methodological approach to brain research. Phenomenological analyses have variable levels of application: They may be less relevant in studies where there are direct attempts at inducing psi (as in #3). Even then, detailed descriptive analyses are still relevant.
Such phenomenological analyses allow non-prejudicial evaluation of subjective interpretations of ostensibly anomalous, psychic or intuitive experiences. Effectively, they apply the medical history-taking approach in assessing psychopathology (e.g., as in analyzing auditory hallucinations phenomenologically).
The
approach neither confirms nor denies the validity of the SPE itself,
suspends judgments of “pathological” versus “normal”, emphasizes
differentiation by phenomenological detail, and may, if extended to
the lab situation, correlate subjective with objective empirical research.
Specifically, detailing SPEs facilitates correlating epiphenomena with
brain localization: Dichotomous descriptions of subjectively interpreted
experiences require careful phenomenological differentiation because
different origins and etiologies could be inappropriately interpreted
as one.
In
2003, Neppe suggested eight methods to facilitate analyzing phenomenological
data descriptions in the brain, namely, detailed data analysis, appropriate
nosological subtype comparisons, specific pathophysiological context,
limitations of single cases, literature comparisons, examination for
unified brain localizations, correlations not implying causality, and
the unproven origins of phenomena.
New principles can be espoused from the above research:
By applying these principles to the above research (#1-3) the limitations of brain reductionism are demonstrable in these SPE and OPE studies. By contrast, approach #4, using phenomenological detail in controlled planned research protocols, demonstrates advantages for such clinical studies, producing more robust results. This is so as these studies can more easily:
Neuroscience
and psi evaluations are complex and the rules should be as fair for
studies of psi and possible anomalous phenomena as they are for all
other scientific disciplines: A baseball analogy can demonstrate how
farcical misinterpretations can be, but such comparisons have their
limitations when referring to psi research.
Detailed Paper:
The hazards of reductionistic
neuroscience interpretation: Revisiting anomalies and subjective experience
linked with the brain.2
(Prof) Vernon M Neppe MD, PhD, FRSSAf, DFAPA, BN&NP, DPM, FRCPC, FFPsych, MMed.
Pacific Neuropsychiatric Institute, Seattle, WA, USA
and Dept of Psychiatry,
St. Louis U., St Louis, MO
Key words basal
ganglia, baseball analogy, bidirectional causality model,
brain, DMILS, extra-sensory perception (ESP), functional MRI (fMRI),
frontal lobe, hallucination, hypothalamus, INSET, near-death experience
(NDE), out-of-body experience (OBE), neurosciences, phenomenology, Possible
Temporal Lobe Symptoms (PTLSs), pseudoparsimony, pseudoskeptics, psi,
REM intrusion, reductionism, subjective paranormal experience (SPE),
temporal lobe, thalamus, Temporal Lobe Questionnaire (TLQ).
Analysis of neuroscience and subjective experience today is controversial. For example, we think we can reduce our complex world of consciousness and anomalous experiences to neurobiological processes in the brain. But can we? Are so-called “out-of-body experiences” artifacts of distorted brain functioning? Can we demonstrate that “out-of-the-body” is actually “in-the-body”? Can we show that the “near-death experience” is nothing more than particular brain activities patterning producing bizarre experiences?
Can we reduce all our “psychic”,
“paranormal”, and “intuitive” subjective experiences to just
a dysfunction of a part of the brain? And can we actually photograph
the changes in our brain that will finally destroy that pesky mythology
that surrounds such terms as “extra-sensory perception”?
Essentially does the success
of modern neuroscience represents the triumph of reductionism? (Lehrer,
2008).
Can we explain ourselves away as a mass of microtubules and a controlled but amorphous, protoplasmic mess. We would then be able to tame the ineffable concepts of “life”, “consciousness”, “reality”, “identity”, “self” and even “creativity”, “genius” and “intuition. ” We would once and for all pack that ghost into the machine and heave a sigh of relief that we need not unthink anything we’ve thought before (Neppe, 2008).
Or maybe we will, once again, doubt that our world is so simple. Maybe we will even look at the cogent evidence that has accumulated over the past quarter century or so, and truly wonder about our origins. Maybe the purely monistic “physicalistic presupposition” will tumble, and we will realize we need to replace our carefully built neurobiologically based edifice or at least augment it.
In this paper, I examine several recent neuroscience research publications that have appeared in the mainstream literature and received media attention. These articles cover alleged psi and their brain correlates. Superficial evaluations of these would apparently support biopsychophysical, reductionistic materialistic models, explaining specific psi experiences purely by brain pathopsychophysiology. Every paper has methdolological strengths and limitations.
I argue that the conclusions reached may not necessarily imply that
explaining psi events as purely brain related events may be insufficient
and that detailed phenomenological analyses and uses of specific cautionary
rules are important.
Overview perspective of these publications.
Five different brain / objective
or subjective psi situations are evaluated.
Effectively, these OBE and
NDE studies evaluated retrospective subjective paranormal experiences
(SPEs) not psi itself as the reports involved subjective experience.
These studies involve attempted
examinations of actual psi (OPE—objective paranormal experience).
Detailed
analysis of these researches (#1-2 and that of Moulton in #3) demonstrate
flaws with commonality of inappropriate methodology and/or interpretations
of applying brain functioning to negate the existence or anomalous source
of alleged psi phenomena, invariably subjectively described.
I
suggest that two other brain models may highlight a more appropriate,
productive approach (#4 and #5):
This paper discusses each of these five areas sequentially.
_____________
Brain Stimulation and the Out-of-Body Experience
“Oh God! I am leaving my body!” (Penfield’s report of a patient receiving temporal lobe stimulation, 1958)
The problem:
The
best way to examine such ideas is to examine the fabric of the subjective
experiences that are among the most threatening to our current worldview,
namely subjective paranormal experiences (SPEs) (Neppe, 1980a).
This is a non-prejudicial term to examine such phenomen allowing evaluation
of what the experient interprets as ostensibly anomalous or psychic
or intuitive experiences but which may not be. SPE has a similar face
validity approach to that used in detailed phenomenological evaluation
of auditory hallucinations (Neppe, 1982a). Applying SPEs neither confirms
nor denies the validity of the SPE itself, and does not label it as
“pathological” or “normal”. Instead, SPE allows for analyzing
links with areas of the brain in order to understand the ultimate expression
of the experience. The approach emphasizes differentiation by phenomenological
detail, and may, if extended, to the present lab situation, correlate
subjective with objective empirical research, just like medical history
taking is used with medical examinations. Specifically, detailing SPEs
facilitate correlating epiphenomena with brain localization: Dichotomous
descriptions of subjectively interpreted experiences require careful
phenomenological differentiation. as different origins and etiologies
could be inappropriately interpreted as one.26
Charles. Tart (1998) pointed out that naturally occurring OBEs are psychologically
important since they are a primary cause of the belief in souls. Whether
the specific findings here will eventually be shown to be part of the
causal mechanism of OBEs is unknown, but future research should study
the full-scale OBE complex, not only the possible component phenomena
(Tart, personal correspondence, 4 November, 2007).
The controversy:
This area has become particularly controversial since the year 2002, when a stimulation of a particular area of the brain (the angular gyrus) in a patient with a right temporal seizure disorder produced the subjective report of the patient saying she was out of her body (Blanke, Ortigue, Landis, & Seeck, 2002). This was replicated on further stimulation. Subsequently, the same researchers (Blanke & Arzy, 2005; Blanke, Landis, Spinelli, & Seeck, 2004; Blanke & Mohr, 2005; Blanke et al., 2005; Bunning & Blanke, 2005) and others (Tong, 2003) have reported stimulation of similar, but slightly different areas of the brain’s right hemisphere (Booth, Koren, & Persinger, 2005) producing these out-of-body experiences. Also, persistent tinnitus (ear-ringing) often was linked with such experiences.
In
fact, such reports are not new. Wilder Penfield in 1958 reported how
he induced such an experience in the brain (“Oh God! I am leaving
my body!”) as did Munro (Munro & Persinger, 1992). And a more
recent stimulation case producing OBEs has been replicated in a patient
with intractable tinnitus who described a “sense of disembodiment”
(De Ridder, Van Laere, Dupont, Menovsky, & Van de Heyning, 2007).
The perspective:
How do we approach these subjective OBE reports? The cited investigations postulated possible brain sites for the OBE, suggesting that the mystery had been solved.
However, some such as Blanke,
acknowledge that they have targeted specific components of the OBE,
not the OBE itself, and are attempting to understand the OBE within
the context of embodiment not trying to ‘explain it away’.
However, when one analyzes OBEs induced by brain stimulation, they are sufficiently atypical to question whether, phenomenologically, they are the same as spontaneously occurring OBEs. In comparison with spontaneous, non-induced OBEs described by Subjective Paranormal Experients (SPEs), they are incomplete in that the whole body is not experienced as being “outside. ” Further, experients of induced OBEs often continue to perceive the environment from the visual perspective of the physical body.
These experients variably produced trivial illusion phenomena (Greyson, 2008): distorted body-image, depersonalization and derealization, visual perceptions of specific fixed location, and other associated parieto-temporal state or trait features. These descriptions differ markedly from thousands of spontaneous OBE reports. These OBEs frequently involve extracorporeal awareness with locality-dependent perceptual experiences; clear imagery; polymodal perceptions and profound cognition. The environment (including the body itself) is accurately perceived from an extracorporeal perspective and this disembodied center of consciousness may move about independent of the physical body (Gabbard & Twemlow, 1984; Gabbard, Twemlow, & Jones, 1982). These descriptions are generally reported by individuals with such brain dysfunctions as seizure foci or tinnitus.
Additionally, when analyzing OBEs and for that matter comparable phenomena such as déjà vu, no single localization can be found (Neppe, 1983c; Neppe, 2006; Neppe & Funkhouser, 2006). We can learn from these other experiences, e.g., at least four distinct nosological subtypes of déjà vu exist (Neppe & Bradu, 2006). Similar research on OBEs needs to be performed to determine the subtypes that may exist (Neppe, 2003).
The following method seeks to ensure the phenomenological description of the data and associate it with identified diagnostic or special research groups (Neppe, 2002).
Thus, these dichotomous epiphenomena of subjectively interpreted “out-of-body experiences” require careful phenomenological differentiation. The induced OBE apparently differs from the spontaneous OBE; using one term—OBE—for both endpoint expressions could produce incorrect clustering of different phenomena (e.g., spontaneous OBEs versus complex partial symptoms). Without determining the possible subtypes of OBEs,. different origins and etiologies could be inappropriately interpreted as one (Alvarado, 2000; Neppe, 2002). In this regard, the analysis of spontaneous cases in parapsychology has a long history going all the way back to Louisa Rhine. (1965)
__________
The near-death experience:
Let me show in allegory how far our nature is enlightened or unenlightened. … Human beings living in a underground den, which has a mouth open towards the light and reaching all along the den… they are strange prisoners… they see only the … shadows, …on the opposite wall of the cave… Would they not suppose that they were naming what was actually before them?
If told this were an illusion, would Man not fancy that the shadows he formerly saw were truer than the objects now shown to him? He will take refuge in the shadows which are clearer to him than the truth. … The truth may be nothing but the shadows of images. (Plato).
Is it not possible that the shadow Man sees is his physical reality alone? (Neppe, 1973).
Plato’s
famous cave allegory may be an important warning that brain waves and
other neurobiological measurements reflect very little of what we assume
they do.
The problem:
The
OBE research on brain stimulation is closely linked with similar investigations
of so-called Near-Death Experiences (NDEs), in which individuals report
unusual perceptions and cognitions while near death (e.g., coma, cardiac
resuscitation). These reports vary but have some consistency: the presence
of non-physical beings; tunnel and light experiences; or being out–of-the-body
(Morse, Castillo, Venecia, Milstein, & Tyler, 1986; Sabom, 1980).
Since the initial volley of reports was published by physicians and
psychologists, the origins of these experiences have been debated. The
neurophysiological basis of the near-death experience (NDE) is unknown.
Do they originate with a lack of oxygen in the brain, from a rush of
endorphins (Jansen, 1990), from imbalances of neurotransmitters (Bonta,
2004), or from temporal lobe activity (Neppe, 1989)? How is it possible
that these experiences can occur when memories during coma are typically
lost (Morse & Neppe, 1991; Sabom, 1980; Sabom, 1998)?
The controversy:
One controversy links NDEs to a state of sleep called rapid eye movement (REM) intrusion, dream-like sleep accompanied by sleep paralysis, which may occur during wakefulness or such clinical conditions as narcolepsy (Nelson, Mattingly, Lee, & Schmitt, 2006). Again, many neuroscientists have ostensibly explained this strange experience as purely brain-linked.
The original REM intrusion NDE article (Nelson, Mattingly, Lee, & Schmitt, 2006) has become so significant that is critical to understand its limitations, while also using it as a jumping ground for further research. Nelson et al. argue that NDE phenomena can be explained by REM intrusion, evoked by cardiorespiratory afferents in an arousal system predisposed to intrusion of rapid eye movement activity. They showed that the lifetime prevalence of REM intrusion in 55 NDE subjects compared with an age/gender-matched control group (who also reported sleep paralysis as well as sleep-related visual and auditory hallucinations) was substantially more common in subjects reporting NDEs. These findings argue that under circumstances of peril, an NDE would be more likely in those with a history of REM intrusion, hence promoting subjective aspects of NDE and associated syncope. Suppression of an activated locus caeruleus (involved with norepinephrine) could be central to an arousal system predisposed both to REM intrusion and NDE.
There are methodological problems with this study, however. It had a retrospective design; only 64 patients out of 446 patients, from the large internet site that recruited subjects, responded to the authors. The NDE experients chosen were also people who had contributed their experiences to a website,\Therefore, they may have been more likely to over-endorse questions about unusual experiences, thinking that the investigators were looking for them. Moreover, the NDE-ers’ REM symptoms were compared to a sample of hospital workers who may have been particularly reluctant to admit any accompanying bizarre symptoms. A proper control group would have been comprised of people who had been near death but did not have an NDE.
But
let us assume the sample was adequate for illustrative purposes. We
then have to face these questions: Is the NDE simply an endogenous physiological
phenomenon? Alternatively, does it have implications for the survival
of consciousness after death?
The perspective:
The important challenge to such NDE research is Occam's razor: We should approach anomalous phenomenon in a parsimonious way. However, we must be aware of what Stent has aptly called premature parsimony— a premature conceptual reduction by investigators that can distort our understanding. The object is to find appropriate explanations, not just the simplest. The explanation must be fruitful, explaining all, not just some aspects of a phenomenon.
In the Nelson research, the data are post-hoc (Nelson, Mattingly, Lee, & Schmitt, 2006): They did not compare the NDE-ers' REM intrusions before and after the NDE. Could the NDE-ers as a consequence of their NDEs have experienced neurological insults that increased the rates for a variety of symptoms? Was the REM state intrusion the result of experiencing a NDE rather than the cause of an NDE?
Personally, I believe that this argument but unlikely. The narcoleptic syndrome has sleep paralysis as a major feature. But REM intrusion could also arise during the pre-sleep hypnagogic and post-sleep hypnopompic states, as well as during the cataplexic and diplopic states we commonly see in narcolepsy and certainly during the overwhelming short day-time sleepiness in narcolepsy. The reason for all these links is that the proportions of REM intrusion, as in narcoleptic syndromes (Mignot et al, 2006), seem to have a solid linkage to sleep onset. So there is precedent (Planelles et al, 1997), and I suspect this predisposition is constitutionally based as, in my clinical practice, I have never encountered brain injury producing such changes. But we also see here a variety of other bizarre symptoms such as hallucinatory experiences (Douglass, Hays, Pazderka, & Russell, 1991). In fact, my working hypothesis is that the narcoleptic-like condition correlates with subjective paranormal experiences just as anomalous temporal lobe activity does.
However, there is a terminological aspect in that the term REM intrusion is not commonly used. I suspect it should be limited to demonstrable REM occurring on polysomnography, not based on historical interview or questionnaire data about symptoms. This, in itself, creates a further level of error. If the authors had used the less sexy term "sleep paralysis" as a correlate of NDE, then we might have said "so what?" Sleep paralysis is a major epiphenomenal expression of REM intrusion and the researchers could easily have utilized that term as it was more well known.
But let’s now look at the other side:
There is no immediate reason why we need to spend thousands of dollars on complex equipment when the medical approach has always been primarily based on history and examination. History includes the eliciting of symptoms—those that are occurring at the same time as the feature being examined—as well as trait signs, in which any symptoms or features that occur over an extended period or even a lifetime are examined, but which do not occur, for example, with either sleep paralysis or NDEs. In the Nelson study only trait features were examined, limiting interpretations of the links with medical conditions or changes in specific foci of the brain. Additionally, as with almost all models, the unidirectional approach was used: near death experients were evaluated for their REM intrusion symptoms by medical history. The bidirectional approach would examine, for example, those patents presenting with REM intrusion features as well as looking at NDE correlates.
This approach is examined further in the next section.
Woody Allen used to joke that he'd been thrown out of college as a freshman for cheating on his metaphysics final. “I looked within the soul of the boy sitting next to me,” he confessed (Saletan, 2007).
This anecdote, if true as attributed, may simply reflect Allen’s humor. On the other hand, it introduces the new phase of functional MRI scanners: Does our very being amount to a mass of microtubules?
Finally, I discuss the most recent catalyst for this paper: the attempted imaging and visualization of the sublime. Research has become even more sophisticated with a Harvard report that a functional Magnetic Resonance Imaging (MRI) study attempted to demonstrate whether or not ESP exists (Moulton & Kosslyn, 2008).
In functional MRI (FMRI) studies, we attempt to demonstrate the functional (as opposed to anatomical) correlates of certain physiological changes, e.g., thinking, hallucinations, delusions, changes in emotion. We can experimentally study, for instance, the brain’s expression of what happens when people laugh or cry. The technology is truly remarkable, but still in its early stage, and the imaging resolution of functional change will no doubt increase enormously over the next several years.
The
Harvard researchers argued that their special methodology was the first
to actually demonstrate that ESP does not occur since it would
have to be processed by the brain. And they could find no difference
between brain activity of their research participants attempting to
elicit telepathy, clairvoyance, and precognition compared with brain
activity of a control group. Superficially, the research looks persuasive
until re-examining the “new method” and the conclusions drawn, and
until re-examining the significant but unmentioned literature on the
positive results already obtained.
The controversy:
In the Harvard study, functional magnetic resonance imaging (fMRI) was used in an effort to document the existence of ESP. The researchers believed that fMRI would be more sensitive than using indirect behavioral methods and designed an experiment that they felt would increase the sensitivity of eliciting positive results for telepathy, clairvoyance, and precognition.
Statistical results overall hovered around the expected chance score of 50%. The researchers concluded that there was no fMRI difference when the participants attempted to evoke ESP compared with participants who were making no such attempt. Does this conclusively prove that ESP does not exist? "No," says the principal author, Moulton. “You cannot affirm the null hypothesis. But at the same time, some null results are stronger than others. This is the best evidence to date against the existence of ESP. Perhaps most important, this study offers scientists a new way to study ESP that avoids the pitfalls of past approaches” (Lavoie, 2008).
Ironically,
if they had found a change, would that change have reflected all types
of ESP or just one specific kind, because their complex design reflected
different tests for so-called “contemporaneous telepathy,” “contemporaneous
clairvoyance,” as well as precognition? Also how specific would such
changes have been? And would they have been characterized only in terms
of correlations, not demonstrable cause and effect? These issues are
relevant to the other studies below, but not to the chance results of
the Moulton study (Moulton & Kosslyn, 2008).
The perspective:
There are, unfortunately, major problems with the Moulton study. However, the methodology was innovative, possibly too much so because the study did not integrate lessons from previous research in the area, nor important theoretical applications such as “psi conduciveness” (Braud & Braud, 1973).
The researchers did not find above-chance ESP scores in 15 of the 16 pairs they tested— the home run (demonstrable ESP) was not hit. But absence of ESP means they could not claim to have studied the phenomenon, and all they could legitimately report regarding those 15 pairs was that there was no physiological change. The correct ESP scores could have been due to chance, and fMRI changes would not have been expected.
However, paradoxically, even if a home run was hit, and there were still no physiological changes, this would not have negated ESP either. It would have just meant that the researchers had not located the endpoint anatomical correlates.
Ironically, Moulton just may have hit a home run—unexpected changes on the fMRI. The sixteenth pair, the only pair demonstrating above-chance ESP scores, yielded provocative results (i. e., less activity in several brain areas with most reduction, notably, being in the temporal lobe) during correct ESP trials as compared with incorrect ESP trials. The researchers explained this away as a “scanning artifact” and concluded the results were not relevant. While this explanation could be correct, this finding could also be associated with ESP, which is elusive even in a laboratory. Paradoxically, the Harvard researchers, therefore, may have explained away their one positive result! This fact makes the remainder of their interpretations questionable. If one positive result can be explained away, why is it not possible to explain away 15 negative results (Radin, 2008)?
The researchers used biologically or emotionally related participants and emotional stimuli in an effort to maximize experimental conditions that are purportedly conducive to psi. These may be legitimate additions. But, there is no precedent justifying why the Harvard experimental procedure, which is complex and untested, might work at all. This methodology, though original, lacks adequate precedence in the literature to justify why the procedure would differentiate ESP versus other elements in fMRI studies.
Important, too, are effects of the subjects’ expectations, degree of psi conduciveness of the psychological conditions (Braud & Braud, 1973), and experimenter effects. These factors may dampen or accentuate results (Green & Thorpe, 1993; Neppe, 1982b), but were apparently not considered by the Harvard team.
Also, the signal to noise ratio in fMRI studies (Logethetis, 2003) may be a legitimate explanation of negative results. If research participants are asked to think about an apple and an orange, the fMRI scans may demonstrate no differences between the two types of events. They are still different thoughts, bur are not demonstrable because fMRI design is potentially insensitive to subtle psychological effects. Similarly, ESP testing involving physical sensory stimuli may produce the same fMRI pictures as the sensory stimuli or absent pictures. A positive result could be camouflaged because it looked the same as the control result, as the same brain areas may be involved and registrations could conceivably resemble normal processing. The ESP signal the Harvard researchers sought with their novel set up may not have been recordable with this kind of apparatus. Therefore, even if so-called ESP demonstrably occurred, Moulton may not have measured it with the correct instruments.
The Harvard researchers did not cite the literature on ESP and fMRI. Later, Sam Moulton asked the parapsychological researcher, Dean Radin, to delineate the literature they had missed. Radin (2008) cited several positive fMRI studies relating to ESP (e.g., Bierman, 2000; Radin, 2006a; Bierman & Scholte, 2002; Richards, Kozak, Johnson, & Standish, 2005; Standish, Johnson, Kozak, & Richards, 2003). In addition, Achterberg, Cooke, Richards, Standish, Kozak, and Lake (2005) examined purported “distant healing intention” using 11 self-identified “healers” and a “sensitive partner” selected by each “healer. ” The healer’s “intention” conditions were significantly correlated with “bold” signals in in most of their partners’ fMRIs while the healers sent ‘distant healing intention” at “on and off” random periods (Achterberg et al, 2005).
Results from the initial Standish pilot experiment to test the feasibility of using an EEG experimental design for an fMRI study were positive, indicating that an increase in blood oxygenation (p< 0. 001) level was observed in the visual cortex of the non-stimulated subject. This was correlated to the stimulus-on condition of the stimulated partner. No such signal was observed when the stimulated partner was presented with the stimulus-off condition or when the subjects reversed their roles (Standish, Johnson, Kozak, & Richards, 2003).
The Richards experiment (Richards, Kozak, Johnson, & Standish, 2005) represents a replication of the use of fMRI technology and the EEG. Extreme care was taken to isolate the subjects from each other and to automate the experiment to avoid any added experimenter error.
There are still limitations, e.g., limited sample size. But because a correlated signal could be detected and replicated in the non-stimulated partner by using two independent neurophysiologic measures of brain function (EEG and fMRI), the evidence is strong that an anomalous phenomenon (not just a recording artifact) may be at play (Richards, Kozak, Johnson, & Standish, 2005). Interestingly, brain changes occurred with the flashing 6Hz stimulus, despite it not being detected by the subject visually.
Further replications can occur either with larger samples or using self-designated “healers”; Achterberg preferred the latter. In that study (Achterberg et al, 2005), significant differences between experimental (send) and control (no send) procedures were reported (p= 0. 000127). Areas activated during the experimental procedures included the anterior and middle cingulate area, precuneus, and frontal area.
In Bierman’s (2000) most complex study, 8 experienced meditators (and members of a control group) were randomly shown images. The time-course of response measured by qualitative analyses (peak counting) demonstrated dynamic changes on fMRI (a “presentiment”) about 4 seconds prior to actually being exposed to some of the emotionally stimulating (either violent or erotic) pictures. During meditation, “presentiment” was significantly linked with erotic stimuli; while the non-meditators’ “presentiments” correlated more highly with violent pictures (Bierman, 2000; Radin, 2006a).
A problem with such “presentiment” research is one of interpretative difficulty, the most radical being “retrocausality,” a backward shift in cause-and-effect. Alternatively, some writers consider “immediate precognition” and other explanations at quantum levels. The problem is that neuroscientists can as easily claim that “presentiment” is, in fact, an expression of the same physiological event measured a fraction of a second prior to its registered actualization (Wegner, 2003).
These
studies are in their infancy and none of their authors issued press
releases claiming they had demonstrated the reality of ESP. In fact,
these authors simply stated that more research was warranted. Moulton
and Kosslyn (2008) published their paper (accompanied by a Harvard press
released) apparently unaware of the previous studies – which, interestingly
enough, were all published by peer-reviewed journals and indexed in
Medline.
The temporal lobe and subjective paranormal experience.
But it is a miserable thing for a question of truth to be confined to mere presumption and counter-presumption, with no decisive thunderbolt of fact to clear the baffling darkness. William James (1896).
Reducing a system to its parts and discarding the critical synergism and Gestalt relationships may lose perspective. Reductionism in science is an appropriate methodology, but it must include complex and possibly, at this stage, ineffable concepts such as "reality," “self and identity,” "consciousness," and even “life” itself (Neppe, 2009, in press).
We must continue to study these topics empirically and in controlled laboratory settings being careful to recognize our interpretations as limited and without prematurely applying theoretical paradigms to the results available. Sometimes that laboratory setting is simply the clinical medical evaluation, but this, too, can yield valuable data.
The clinical symptomatology approach has been a fruitful direction of interest for the neuroscience researcher. One benefit is that it is much less expensive than apparatus such as Functional Magnetic Resonance Imaging, which can be extremely cost. Hence, sample size can be much larger, and more clinical parameters can be measured.
This approach emphasizes the phenomenological aspect of neuroscience, examining symptoms and clinical features so they can be correlated with the particular subgroup being analyzed. For example, detailed information on olfactory hallucinations can be correlated with temporal lobe epilepsy (Neppe, 1983a, Neppe 2009 in press).
This approach also illustrates the bidirectional model of causality. It applies what has been an unrecognized but standard medical model for centuries by allowing statements about correlations to reflect either a cause, an effect, or both.
Are such subjective paranormal experiences (SPEs) merely a manifestation of the brain playing tricks on us? If so, is there an area of the brain where these tricks occur?
Our understanding of SPEs from a physiological point of view would be greatly enhanced if we could pinpoint a section of the brain in which psi (e.g., ESP, psychokinesis) mediation occurs, or at least an area that plays a primary role. Such knowledge would provide at least three concrete benefits.
We can apply these same analogies directly to psi and the brain. Can we use a methodology based on the clinical medical model to assist our studies here? Let me whet your appetite by briefly discussing my own research on the temporal lobe, which, with respect, pioneered this approach in the context of SPEs (Neppe, 1980b, 2003).
This research required the development of a measuring instrument, the Neppe Temporal Lobe Questionnaire (TLQ), to elicit symptoms that could be attributed to the temporal lobe of the brain. These were called Possible Temporal Lobe Symptoms (PTLSs). Our later work used an upgrade of this instrument, the INSET (Inventory of Neppe of Symptoms of Epilepsy and the Temporal Lobe) (Palmer & Neppe, 2003, 2004).
Similarly the research required development of measures to screen for so-called “psychic experiences” and thereafter to go into great detail to elicit whether subjects had spontaneous SPEs and to use criteria for levels of subjective validation of the experiences. Again, in no way does this imply the experiences objectively occurred as interpreted. The essence of such phenomenological research is to be non-prejudicial and to approach experience in the same way as one would approach subjective reports of pain, dizziness, or hallucinations. There are ways of quantifying experience, and this approach offers the ability to develop comparative experimental and control groups. In our later work, the INSET incorporated such data.
The original work was my retrospective pilot study in South Africa. This examined whether more possible temporal lobe symptoms (PTLSs) are associated with ostensibly normal subjects claiming a large number of SPEs than with subjects claiming none, and if so, whether any specific PTLSs stood out. Both state and trait symptoms were examined. If PTLSs occurred during or just before or after the SPEs then this would be a Temporal Lobe / SPE state; conversely, if they occurred at other times (as with the Nelson research on REM intrusion), these would be trait phenomena that may imply a constellation of several symptoms.
In the initial Neppe study, despite a small endpoint sample size, SPE Experients exhibited significantly more PTLSs than SPE Nonexperients (p<0. 001), with olfactory hallucinations being particularly common. These findings suggest an anomalous kind of temporal lobe functioning among the SPE Experients, but neither confirm nor deny the veridicality of their SPEs. This work is theoretically very important: For the first time since Descartes misrepresented the pineal gland, an anatomical area could reliably be regarded as a kind of interaction zone for mind and brain—whether or not that “mind” may still be brain or allow an appreciation of such experience.
Subsequently, this work was replicated in a different population by Michael Persinger in Canada, again in normal populations (Persinger & Valliant, 1985). I did further work on SPE Experients demonstrating a detailed qualitative kind of olfactory hallucination that overlapped with PTLSs but were also different (Neppe, 1983a): the particular type of olfactory hallucination associated with SPEs has a pleasant and perfumy odor but commonly co-exists with unpleasant burnt-smelling or foul-smelling temporal lobe type hallucinations. Similarly, I extended this work to the déjà vu phenomenon demonstrating that there were at least four qualitatively distinct, homogeneous categories of déjà vu (Neppe, 1983c):
A study in this direction was our analysis of two families with ostensible psi abilities and temporal lobe dysfunction (Hurst & Neppe, 1981, 1982). This study may suggest familial links to temporal lobe syndromes combined with SPEs. However, case reports may reflect exceptions, and the data are only suggestive.
These kinds of findings reflect correlations only. To establish a higher probability of causality one needs bidirectionality. This means using a novel methodology by applying the two converse rules:
My
colleague, John Palmer, and I did this. This time, we were able to demonstrate
that those with temporal lobe dysfunction have more SPEs than did a
comparative population (Palmer & Neppe, 2003, 2004).
Bidirectionality
This
produced what I call the “bidirectional medical model of causality.
” Effectively, physicians have been applying the “bidirectional
medical model of causality” through the ages. For example, in the
model of malaria, the condition can be diagnosed clinically, and then
confirmed by isolating Plasmodium. Conversely, a malaria diagnosis may
be made based on Plasmodium in the blood and then finding correlates
with clinical malaria. This moves correlation closer to causality. Even
though this is still subjective, the subjective experience model in
no way diminishes attempts to correlate it with objective events. Even
when such causal links like the temporal lobe research (above) are found,
this is just one necessary but insufficient requirement for SPEs
to be expressed in the brain. We may have a functioning brain, but we
still cannot walk without legs.
Even though,this model has
been applied in the practice of Medicine for centuries, tt works but
has its limitations. The limitations are recognized as differential
diagnoses. With each source of diverse information the assessment becomes
clearer but it never attains 100% clarity. The same would apply to SPE
research. Bidirectionality nevertheless remains a promising method of
analyzing relationships in parapsychological research.
Because correlations are not necessarily causal, the bidirectional approach amplifies guidelines to interpret experiences include the bidirectional approach for causality(V. M. Neppe, 2008; Neppe 2008;. Neppe, 2009, In press). Applied in the two converse SPE populations of #4
Lessons from the above research
New principles can be espoused from the lessons of #1-3 above and the phenomenological detail of #4:
By applying these principles to the above research (#1-3) the limitations of brain reductionism are demonstrable in these SPE studies.
By contrast, approach #4, using phenomenological detail in controlled planned research protocols demonstrates advantages for such clinical studies, producing more robust results. These studies can more easily:
The frontal lobes and other anatomical organs: Theoretical bases.
One can certainly argue that the lack of adequate frontal lobe functioning allows reduced self-awareness that may facilitate effects of intentionality on physical phenomena (Dobyns, 2003; Freedman, Jeffers, Saeger, Binns, & Black, 2003). This general state hypothesized by Ehrenwald (1975) allows reception of psi related information from outside (Bergson, 1914) because psi cortical filters are impaired (Neppe, 1990). However, if one looks at the model of temporal lobe functioning, it does not necessarily require dysfunction for individuals to experience significant SPEs.
I have suggested that it requires a different kind of anomalous temporal lobe functioning that may be facilitated or correlated with dysfunction of seizures but may also occur in ostensibly normal SPE Experients.
If one uses the same parallel with the frontal lobe if there is a correlation with psi, this may not necessarily imply a feature reflecting a more generalized dysfunction. In this regard, impaired self-awareness. It does not necessarily involve dysfunction of the frontal lobes even if we find a correlation of frontal lobe symptomatology with SPEs. We would need to use the same bidirectional, causal, medical, hypothetical model to link the two and if so we should examine SPE experients to establish if there are frontal lobe symptomatology links.
This kind of research is critical because I have previously hypothesized that the frontal lobes could correlate with efferent psi (i. e., psychokinetic or PK) function (Neppe, 1990). The logic behind the hypothesis is that psychokinetic abilities are motor / efferent functions. The frontal lobe is the classical executive cerebral cortical organ. It is involved with every level of higher brain motor function. It is the logical candidate either alone or with the anterior temporal lobe for efferent psi phenomena.
Also relevant is the fact that unconscious psi phenomena sometimes occur. How does one measure "presentiment" on an EEG if indeed this is some kind of precognitive phenomenon or even, more radically, retrocausality. How does one measure autonomic changes in percipients correlating these changes with stimuli known only to the transmitters or agents? How does one correlate brain function with so-called spontaneous telesomatic phenomena, e.g., an itchy left foot known to the experient as an indication of danger to the family? Essentially, these same principles apply as described:
All said, if such unconscious psi has occurred, I will make some further predictions: the logical brain organ for such a correlation is the thalamus for afferent unconscious psi (as in so-called ESP) and for the hypothalamus to refer to endocrine linked psi, and for an unconscious efferent motor series of cerebral neurons to be involved. One example may possibly be the basal ganglia for unconscious efferent psi (as in so-called PK).
I
will not at this point argue that these are all non-dominant hemisphere
related functions. The brain works holistically in multiple ways.
Analyzing Subjective Paranormal Experiences (SPEs)(Neppe, 1980, 1982) constitute a major methodological approach to scientifically assessing #1 and #2, and to apply detailed phenomenological methods to #4 and #5. SPE analyses are less amenable to #3 where the attempts at that moment of inducing psi are paramount, somewhat analogous to the medical examination, but even then detailed descriptive analyses are still relevant.
Neuroscience and psi evaluations are
complex and the rules should be fair for these as with all other scientific
disciplines: A baseball analogy can demonstrate how farcical the misinterpretations
can be but such comparisons have its limitations because different scientific
endeavors have different levels of proof. Whereas there is a significant
body of literature in regard to parapsychological research, there are,
as with psychology and the neurosciences, difficulties with ecological
validity in that samples, conditions and methodologies frequently vary
even in minor format.
I use the following comparison using a baseball analogy. I am deliberately being farcical because it illustrates so well the problems of methodology, the need for detail, the complexities of interpretations and the ostensible double standards. I’m a great admirer of Ken Griffey, Jr., whose career began in Seattle, so choosing him in this farce reflects my admiration for this baseball icon.
Let us suppose that we want to examine the brain correlates of Griffey’s home-run swing. Griffey is appropriately tested with the most sophisticated apparatus around. But he does not hit a home run. Do we conclude that there is no change in his brain during his home run swing? Of course not.
But many critics often do this with psi.
Now we test him again. This time he hits a home run. Our apparatus shows some change, but we find that this same change occurs during other states that others have exhibited. Do we conclude that he hasn't really hit a home run because others who don't hit home runs also show that change? Of course not. Or do we say: We will study a large sample of home runs and compare it with a large sample of non-home run swings in which he made an out? Fair enough. We may find Griffey shows no demonstrable change.
Do we conclude that his home run swing does not really exist? After all, we cannot demonstrate it in the brain. Of course not. We know it exists. We may say that our specific apparatus is not sensitive enough to differentiate his home run swing from his non-home run swing.
But many critics do this with psi.
Now, Griffey hits a home run again. This time he exhibits some unique change. The researchers notice it is one specific kind of home run he hits, only the longer ones to the left side. They are proud that they are realizing there is a need to subtype this “kind” of home run.
These data are excellent. Researchers realize that they need to qualitatively differentiate subtypes as we must with research in SPEs.
They conclude that they need to study this specific feature more extensively, otherwise how do they know these specific home run findings really are linked with the brain changes? This seems legitimate but time consuming and difficult. But they have the financial resources to fund it, so they go ahead. They allocate complex mathematical analyses (e.g., multidimensional scaling, correspondence analyses) to ensure that they understand the differences between the subtypes they have analyzed.
And in fact, I used multidimensional scaling in 22 dimensions to examine the déjà vu phenomenon in great detail and to demonstrate correlations of particular kinds of déjà vu with specific subtypes (Neppe, 2006; Neppe & Bradu, 2006; Neppe & Funkhouser, 2006).
Critics might think: "Wow, if we study psi we might have to subclassify some events as well. ” But they quickly put that out of their minds because they know psi phenomena don't exist.
Now the researchers want to replicate their study. Replication is key in research. The difficulties often relate to exact conditions being replicated.
They know there is a complex system of neurobiology at work and maybe even a dogged anomaly that they cannot measure. They may even realize this is anomaly is correlative, not causal.
But if these were SPEs would they conclude that the brain changes are the causal links for the specific SPE features indicated? They look at the cited research on stimulating the brain and producing OBEs, on REM intrusion causing NDEs, on fMRI showing or not showing any kind of ESP, and wonder why causality rather than correlations were emphasized. They also examined the temporal lobe and its links to SPEs and noted the care taken to emphasize correlations, not causality.
The researchers would, of course, not conclude that Griffey's home runs actually do not really exist and are instead fantasies and imaginings. They know there are independent spectators who saw these home runs, and that they are not just mass hallucinations.
Yet, bizarrely, many critics do all of this regarding psi, even when statistical data for methodologies achieve unbelievable levels. Rejecting all that evidence for their conclusions would be as ridiculous as saying Griffey’s home runs were not hit instead of saying “We don’t quite know in what way they were hit. ”
What can we conclude? Can we say that a certain pattern of brain function allows individuals to hit home runs? No, after all this, we cannot even say that.
All we can say is that there appears to be a correlate of a distinct pattern of brain functioning when individuals strike the ball hard enough to hit a "special" kind of home run. This neither demonstrates nor denies the causal link of the underlying subjective experience of the hitter, or the objective brain experience that the individuals concerned may have when they hit a home run. Indeed, when a home run is hit far more than cerebral cortical mechanisms are involved. A whole, possibly perfectly synchronous sensorimotor loop is involved in the properly trained individual. That one tiny finding in the brain in this extensive study may be simply an epiphenomenon of something far more complex.
And
so the researchers learn about the utter complexity of the real world,
and the difficulties of doing such research -- and the focus they need
to only measure home runs.
Perspective:
Let's just substitute one word here. Instead of “home runs” let us apply the same framework to “psi”.
The
paradox is that only in a discipline such as this—the discipline commonly
called “parapsychology” (a discipline I believe should more correctly
be called “dimensional biopsychophysics”)—would critics dare to
write without assiduous examination of the appropriate literature--and
succeed with approbation?
Conclusions:
Neuroscience
and psi evaluations are complex and the rules should be fair for these
as with all other scientific disciplines: A baseball analogy can demonstrate
how farcical misinterpretations can be but such comparisons has its
limitations because whereas visual observations in a baseball game and
its rules are universal, the occurrence and implications of psi phenomena
involves an area of ongoing research and study. Nevertheless, I believe,
the discipline should be accorded the same objective respect in these
analyses as other areas of science.
Arthur Koestler (1959) summarized the situation: “Innovation is a two-fold threat to academic mediocrities: It endangers their\ oracular authority; and it evokes the deeper fear that their whole laboriously constructed intellectual edifice may collapse. '”
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I wish to thank the several
readers of this article as well as Pacific Neuropsychiatric Institute
which retains intellectual property rights and copyright for permission
to publish.