A Controlled Analysis of Subjective Paranormal Experiences in
Temporal Lobe Dysfunction in a Neuropsychiatric Population
By John Palmer and
Vernon M. Neppe
Palmer J, Neppe, VM . A controlled analysis of subjective paranormal experiences in temporal lobe dysfunction in a neuropsychiatric population. Journal of Parapsychology, 2003, 67:1, 75-98.
Our thanks to the Journal of Parapsychology for permission to republish this.
The research was supported by an international Bial Grant funded from Portugal.
A companion article is :
Palmer J, Neppe, VM, Exploratory Analyses of Refined Predictors of Subjective ESP
Experiences and Temporal Lobe Dysfunction in a Neuropsychiatric Population.
European Journal of Parapsychology, 2004, 19, 44-65. we link here to the landing page.
These two critically important papers extend the original research of Drs Neppe on subjective paranormal experience and the temporal lobe demonstrating anomalous temporal lobe functioning is both state and trait related to subjective paranormal experience.
Neppe VM. Temporal lobe symptomatology in subjective paranormal experients. Journal of the American Society for Psychical Research . 1983; 77 (1): 1-29 (not yet available on the Internet)
ABSTRACT: This research extended
to a neuropsychiatric population findings by Neppe and by Persinger that
subjective paranormal experiences (SPEs) are associated with temporal lobe
dysfunction (TLD) in the brain. The
sample consisted of 100 of Neppe’s patients at the Pacific Neuropsychiatric
Institute in Seattle, WA. TLD was
defined as a composite of 4 diagnostic criteria: (a) symptomatology as measured
by 16 TLD-specific items from Neppe’s INSET questionnaire; (b) predisposing
conditions (recreational drugs, brain damage); (c) anomalous
electroencephalographic (EEG) activity; and (d) response to anti-convulsant
drugs. SPEs were measured by questions on the INSET referring to ESP,
apparitional, and out-of-body experiences. TLD criteria and SPEs were coded
independently by 2 raters, each of whom were sent portions of patient files
from which information relevant to the other rater had been removed. 60 patients classified as having TLD had
significantly more SPEs than 27 patients who were not (p<.05, one-tailed). 13 borderline patients on TLD were removed.
Supplementary regression analyses revealed that this result was due entirely to
symptoms (INSET) as predictor (p <
.001). Females reported significantly
more TLD symptoms and SPEs than males, but this confound did not destroy the
INSET-SPE relationship. Phone interviews
of 20 patients reporting SPEs confirmed that the great majority had at least
one credible ESP experience.
Our understanding of psi
from a physiological point of view would be greatly enhanced if we could
pinpoint a section of the brain in which psi mediation occurs, or at least an
area that plays a primary role. Such knowledge
would provide at least three concrete benefits. First, by considering the
functions performed by this part of brain, we could develop more incisive
insights about how psi manifests. For
instance, if the area plays a crucial role in the activation of memories,
credence would be lent to the hypothesis that psi occurs by activating stored
memories (Roll, 1966). Second, if
momentary brain states could be found to correlate with the accuracy of
discrete psi responses, progress could be made in predicting which particular
psi responses (e.g., guesses on a card test) will prove to be correct. Third, attempts could be made through
biofeedback, drugs, or other means to alter the functioning of this part of the
brain to enhance psi performance.
The earliest example of an
exploration of the relation between SPEs and the temporal lobes is an
uncontrolled study by Nelson (1970), who found that 10 of 12 trance mediums had
evidence of temporal lobe instability in their EEGs. Subsequently, Nelson and
Neppe (1980) did not replicate these EEG findings in the population from the
South African Society for Psychical Research (SASPR) studied by Neppe (see
below). Roll (1977) suggested a link
between epilepsy and poltergeist activity, based on the fact that 22 of 92
persons regarded as the foci of such activity that he surveyed were prone to
“seizures or dissociative states” (p. 400).
In one particularly noteworthy case (Solfvin & Roll, 1976),
poltergeist outbursts appeared to alternate with seizures in a grand mal
The first controlled study
to investigate the relationship between temporal lobe instability and SPEs was
by Neppe (1979, 1980b, 1981a, 1982, 1983b), who analyzed the SPEs reported by
all members of the SASPR. He found that
a core group of six members reported large numbers of SPEs according to
pre-stipulated criteria. These persons
had significantly more possible temporal lobe symptoms than a group of six
control subjects from the same society who reported no SPEs. Data were collected from interviews and
detailed questionnaires. The latter
included the Neppe Temporal Lobe Questionnaire and several SPE questionnaires,
derived in part from a questionnaire developed by Palmer (1979). These instruments were administered to
subjects verbally. The findings
demonstrated a link of temporal lobe functioning to SPEs at both a state and a
trait level, and also suggested a link of seizure type phenomena with these
Neppe later delineated a particular type of olfactory hallucination
associated with SPEs that is pleasant and perfumy but commonly co-exists with
temporal lobe type hallucinations (Neppe, 1983c, d). This again supported the trait link of
temporal lobe firing with SPEs. Finally,
he demonstrated that the temporal lobe epileptic, the subjective paranormal
experient, the psychotic, and the normal subject each describe a specific
subtype of déjà vu experience (Neppe, 1981a, 1983a).
Persinger has published extensive research and theorizing on the role
of the temporal lobes in psi experiences. He attributes SPEs to instability or
micro-seizures in the temporal lobes, particularly the hippocampus and amygdala
(Persinger, 1989). He tested this
hypothesis by giving a 29-item scale of temporal lobe symptoms and a scale measuring seven different types
of SPEs (including telepathy, out-of-body, and spiritual experiences) to groups
of 108 and 41 college students (Persinger, 1984). These scales were a direct derivation of
Neppe’s original Temporal Lobe and SPE questionnaires. (Neppe, 1981a, b,
c) In both samples there were
significant positive correlations between scores on the temporal lobe scale and
number of different kinds of SPEs reported. This research was replicated and
extended with a sample of 99 college students, who were given a 16-item scale
measuring complex partial epileptic signs (CPES) in addition to the scale used
previously (Persinger & Vaillant, 1985).
Both scales yielded significant positive correlations with the number of
different kinds of SPEs. It is also
noteworthy that persons engaged in artistic professions score high on
Persinger’s temporal lobe scales (Persinger & Makarec, 1993) and also show
exceptionally positive results in ESP Ganzfeld experiments (Palmer &
Persinger’s TL scales have
been validated in two ways. First, it was
shown that epileptics score substantially higher than controls on the scales
(Persinger & Makarec, 1993). Second, amount of EEG alpha activity in the
temporal lobe, but not the occipital lobe, was greater among high than low
scorers on Persinger’s scales (Makarec and Persinger, 1990). However, the scales do not show particularly
good discriminant validity as measures of temporal-lobe epilepsy. Clinical groups suffering from post-traumatic
stress disorder, anxiety-depersonalization, and “exotic dissociation” scored
quite high on the scales (although not as high as the epileptics), and the
scales correlate extremely highly (.72 to .83) with the Bernstein-Putnam
Dissociative Experiences Scale (Persinger & Makarec, 1993).
All the above data involving the relationship
between temporal lobe symptoms and SPEs were collected from normal
populations. If the relationship between
these variables is truly linear, one would expect temporal lobe epileptics to
have even greater amounts of SPEs than normals who happen to score high on the
kinds of scales discussed above.
However, this remains to be established.
Persinger (1989) argues that repeated epileptic motor seizures destroy
brain tissue and thus might actually reduce the incidence of SPEs. Sensky et al (1984) found no tendency for diagnosed temporal lobe
epileptics to have more mystical experiences than control groups of primary
generalized epileptics and patients suffering from migraine. However, the samples in each were group were
small in this study (N < 30) and
the measurement of SPEs did not appear to be very thorough. Also, Hurst and
Neppe (1981) have described a familial link between seizures and SPEs and as a
consequence developed the term “psi-genetics” (Neppe & Hurst, 1982). Clearly, more research is needed to settle
An opportunity to derive more information from clinical populations is
provided by Neppe, who sees many temporal lobe epileptics in his clinical
practice at the Pacific Neuropsychiatric Institute in Seattle. He collects enormous amounts of data from
each individual, including etiology, current symptoms, EEG data, and responses
to anti-convulsant (A-C) drugs. His
symptom questionnaire includes questions
on SPEs. This Short
Inventory of Neppe of Symptoms of Epilepsy and the Temporal Lobe (INSET)
serves as the basis for detailed analysis of every positive reported symptom of
temporal lobe disease, based on criteria developed initially by Neppe (1979,
1981 a, b, c) and later by Neppe and
Tucker (1988, 1992).
Although it is Neppe’s
subjective impression that his TLD patients have an unusual number of SPEs and
more than his other patients, time constraints have prevented him from
analyzing these data quantitatively. The
purpose of the proposed project is to remedy this deficiency through a
collaborative effort involving other qualified individuals who have the time
and expertise to complete the task.
Selection of Patients
The initial plan was to evaluate 80
patients and to do a preliminary analysis of the hypothesis after the first
40. However, it soon became apparent
that a larger proportion of patients were falling into the TLD group than was
anticipated, raising the concern that the control group would be too small to
properly analyze. It was thus decided to
raise the total sample size to 100 patients and forgo the preliminary
analysis. Palmer (JP) and Neppe (VN), who at the time were blind to the
patients’ SPE scores, made this decision.
Neuropsychiatric patients (with
neurological as well as psychiatric symptoms) were selected from among those
seen within the previous 6 months. In
most cases, follow-up sessions with such patients were anticipated. The folders
of these current patients were already arranged alphabetically by last name in
the files. Patients were entered into
the sample sequentially. An initial batch of 75 patient files passing the
original cut was selected by VN.
Additional batches totaling 36 files were later supplied to the raters. The latter batches consisted of cases VN had
just completed reports on and were selected in the order of the report
completion. Thus, they were more recent
than the first batch. The total number
of patients exceeded 100 because 11 cases were later found to be invalid and
had to be replaced. 8 of these were found
to have met the exclusion criteria, and 3 were found to be duplicates of
first-batch patients that mistakenly crept into the subsequent batches.
All patients included in the sample
gave informed consent to have their files used for the research. Only 6 qualifying
subjects were excluded prior to processing because of absence of informed
consent. Prior to inclusion in the original sample, VN also excluded cases that
he knew met the following exclusion criteria: (a) under age 18 as of 1/1/2000,
(b) electroconvulsive therapy within the past 6 months, (c) a major
psychological disorder (mental retardation, active psychosis, dementia or
malingering), and (d) insufficient investigation despite full reports: this
usually involved absence of EEG data during the evaluation or in the preceding
six months. Approximately 15 to 20 cases
were excluded by these criteria.
of Computer Files
At the outset, to preserve
anonymity, the names of patients were converted to their initials plus a digit. VN’s Microsoft Word computer files of his
patients are extensive, ranging in size from about 40 to about 120 typed
pages. Only some of the information in
the files was relevant to the coding criteria.
It was decided to have JP code the files for neurological problems and
Nebel (HN) for SPEs and to keep each rater blind to the material coded by the
other. To facilitate this blindness, the
files were edited to remove references to SPEs from the files sent to JP by
using the “find” command in Microsoft Word.
Likewise, information about TL and seizure symptoms was removed from the
files sent to HN. All this editing, including the removal of
patient names, was done by HN for the 82 patients and by Magill (SM) for the
last 18 patients. These files were then checked by VN to ensure
that the editing was done properly.
It was admittedly less than ideal
for HN to edit the initial 82 files for neurological information, as this was
the information she was supposed to be blind to. Unfortunately, staff time and
number of staff assigned to the project required this arrangement. To mitigate the problem, HN edited by removing whole sections located by the
Word “find” command without reading them, deliberately did not read the folder
at all thereafter, and edited the whole set such that her own seeking of SPEs
was done at a time weeks or usually
months later when she regarded herself as blind. In general, both raters (HN and JP) were
instructed to look only at the particular sections of the files containing the
information relevant to their respective rating tasks.
4 specific classes of diagnostic information that the raters used to assess
whether patients were to be assigned to the TL group or to the control group.
They will be described briefly below.
INSET. The Short form of
the Inventory of Neppe of Symptoms of Epilepsy and the Temporal Lobe (INSET) is
designed primarily to assess behavioral and subjective symptoms characteristic
of TLD and seizures. The part of the
INSET relevant for present purposes is a series of 53 multiple-choice
questions, each representing a symptom or class of symptoms characteristic of
neurological disorders of various kinds.
Each question has 7 response choices representing frequency of
occurrence. They are: (0) “never”; (1) “less than once per year”; (2) “yearly
or more”; (3) “monthly or more”; (4) “weekly or more”; (5) “daily”; and (6)
“more than daily”. In some of the results found in the computer files, a
different set of response alternatives is sometimes reported that translates to
the preceding set according to the following transformations: (1-2) “rare”; (3)
“occasional”; (4-5) “frequent”, and (6) “very frequent”. All questions are asked both for “recent
experience” and for “past experience”.
Of the 53 questions, only 16 refer
to symptoms specifically characteristic of TLD.
These questions, listed in the Appendix, were the only ones used for TLD
classification. In addition, at the end
of the INSET are 4 questions referring to SPEs that were coded for this
project. Specifically, they address ESP experiences, out-of-body experiences
(OBEs), and apparitions. These
questions, which provided the SPE scores, are listed at the bottom of the
Patients completed the INSET during
their first or second visit to PNI.
After completing it, VN interviewed them about their responses to each
question they answered affirmatively or were unclear about, to elicit further
information and to be sure the question was understood as intended.
Neither the short INSET nor the
16-item subscale used for this research has undergone psychometric evaluation.
One purpose of this research is to provide such data, particularly the internal
reliability of the 16-item subscale (hereafter referred to simply as the
During the initial interview, summarized in
the file under a section labeled “History of Main Complaint”, and as part of
the INSET, patients were asked if they ever had a head injury or a brain
disease such as encephalitis or meningitis, brain surgery, or brain tumor. They were also asked about the past and
current frequency of recreational drug use.
The specific drugs inquired about are marijuana, LSD, mescaline,
amphetamines, cocaine, phencyclidine (PCP), heroin, narcotics, alcohol,
caffeine, tobacco, and the ever-present “other”. These results are summarized
in a table in the files labeled “Abuse History” and summarized briefly in the
report of the INSET.
EEG. Patients at PNI are very commonly evaluated
electro-encephalographically. Depending on clinical indications, they receive
either or both of:
18 channel wake and sleep EEGs including activation
procedures of hyperventilation and photic stimulation .
2 to 3 days of 16 to 18 channel computerized home ambulatory EEG
monitoring with an ongoing record of the patient’s brain waves during waking
activities as well as sleep. The
technology used is possibly the most sophisticated home EEG monitoring system
in the world, namely the Sleep-Wake DigiTrace apparatus. To accentuate the
clarity of records, and diminish outside artifact, playbacks used high digital
frequency filters. At times, when necessary, recordings were slowed to
facilitate more adequate reading and interpretation. Automated seizure computer
files, push-button events, and background EEG monitoring were used and stored
on computer. All tracings were
independently read by an acknowledged world expert on the DigiTrace technology
at Harvard University in Boston. Patients or families would press a pushbutton
when they thought a seizure, spell, event or other anomalous sensation may have
been happening or coming on, and these records were therefore marked and
correlated with the simultaneous brain-wave activity. Because of the referral
pool, VN uses placements to accentuate the temporal lobes most, so as to
extract a higher yield. In this research, almost invariably, a coronal temporal
montage was used, usually with added T1 and T2 electrode placements. Additionally, these patients had
electrocardiographic monitoring to ensure that brain abnormalities were not
occurring concurrently with heart arhythmias.
All but 7
of the100 patients in our sample were given the ambulatory EEG. In 6 of these cases the exclusion was because
the sleeping and waking EEGs were both normal and their were no other reasons
to think the ambulatory EEG might yield a different verdict. In one case, the patient resisted the
ambulatory EEG. The EEG results are
given in a section of the file specifically devoted to them and summarized in a
sub-section under the heading “Diagnosis”.
In a few cases, waking and sleep EEGs were not
conducted at PNI because they had recently been done elsewhere or it was felt
that going directly to ambulatory EEG was appropriate. In these cases, the reports of these earlier
EEGs were considered for the coding.
Response to Anticonvulsant Medications. If the previously obtained diagnostic
information indicates that the patient is experiencing seizures and or is
likely to have TLD, they are generally given one of a variety of anti-convulsant
medications. Whether such a medication
is to be prescribed and the specific medication(s) of choice are listed in the
files under a section called “Specific Recommendations”. Response to these medications is documented
in the reports of follow-up visits the patients make to PNI. The number of such visits reported in the
files varies greatly from patient to patient, depending in large part on the
recency of the initial visit. It is common for the dosage level of the A-C
medications to be varied over time, and sometimes patients are changed from one
A-C to another. These changes are
usually dictated by the effectiveness of the current regimen in ameliorating
the symptoms and also the presence of side effects. It is common for patients to be prescribed
other drugs, such as anti-depressants or anti-anxiety agents, in addition to
outset of the project, VN and JP agreed on a preliminary set of coding criteria
that were followed for the first patients evaluated. However, it eventually became apparent that
some of these initial criteria were producing weird and unrealistic
distributions of scores. For instance,
the initial scoring scheme for TLD symptoms on the INSET produced an overwhelming
proportion of patients given the highest score (3). It was thus decided to
modify the criterion for scoring these INSET questions, most notably by
downgrading symptoms that appeared infrequently. All such decisions were made by VN and JP
based primarily on characteristics of the overall distributions of scores, not
scores of individual patients, and, most importantly, without knowledge of SPE
Symptoms (0 to 3). The frequency
scores on the 16 INSET items devoted to TLD were transformed as follows:
0.25 = 1-2 (rare, yearly or less, etc.)
0.50 = 3 (occasional, more than yearly up to
= 4-6 (frequent, more than
Each item was scored only
once; when the scores for “recent” and “past” differed, the highest was chosen.
The item scores were then summed to yield a total raw score, with a possible
range of 0 to 16, based on the scoring scheme above. The raw scores were then
transformed to the final classification scores as follows:
0 = 0 to 0.75
1 = 1 to 3.75
2 = 4 to 5.75
3 = 6 or higher
(0 to 2). 1 point was scored
if the patient had suffered a head injury, brain tumor, or brain disease (e.g.,
encephalitis). Head injuries only
counted if the patient experienced loss of consciousness, concussion, and/or
1 point was scored if the patient
had a history of using certain recreational drugs. If the frequency of use of any of the
following drugs met the defined standard, the point was scored:
Marijuana: Over many
years or very frequently over shorter periods of time
Hallucinogens (LSD +
mescaline + PCP): 3 or more times
Amphetamines: 6 months
or more, or at least 30 times (unless prescribed)
Opiates: 6 months
or more (unless prescribed and patient not an addict)
EEG (0 to
3). The EEG reports
generally contained information about the number of spikes and paroxysms in the
EEG records, their laterality and focality.
In most cases, the file also contained evaluative statements of the EEG
record regarding its indication of TLD.
In these cases, the following formula was used to arrive at a
classification score for EEG:
0 = “normal”, “do not support” TLD
1 = “mildly abnormal”, “weakly
2 = “abnormal”, “support” or
“moderately support” TLD
3 = “severely abnormal”, “strongly
There were 16 files that did
not include evaluative EEG statements.
JP had guidelines giving some indication of what specific kinds of
abnormalities deserved what scores, but he found this difficult to apply to
specific cases. So he decided to extract
excerpts of the EEG abnormalities recorded in each file, eliminated any phrases
that might identify the patient (e.g., name of physician who had conducted
previous EEG examination), removed the patient initials that identified the
file, randomized the order of the cases, and emailed them to VN. VN then supplied scores for the 16 cases. He
reported that he was unable to identify any of the patients from the material
A-C Response (-3 to 3). The response of patients’ symptoms to A-C
medications was coded on a 7-point scale from “much worse” (-3) to “much
better” (3). Where applicable, separate
judgments were made for seizures and psychological symptoms, and the most
positive result was chosen for coding.
When there were different results for different psychological symptoms,
the average was taken. Side effects,
insofar as they could be clearly identified as such, were ignored for purposes
of coding. Primary consideration was
given to the most recent evaluations and evaluations explicitly linked to an
Patients for whom no A-C
drug was recommended nor given by VN were coded 0. Cases in which an A-C drug was recommended
but not given (e.g., because of a fear of untoward effects like side-effects or
patient resistance) were coded 1.
classification scores were summed over the 4 diagnostic categories (symptoms,
etiology, EEG, A-C response) to yield a TLD score with a possible range of –3
to 11. These were converted to classifications as follows:
6 to 11:
-3 to 4: Control Group
The indeterminate group was decided upon as a buffer
to help protect against misclassification. Patients in this group were
eliminated from the comparison testing the main hypothesis.
Clinical Classifications. As the name implies, the purpose of the above
coding scheme was to give an objective, quantified basis for patient
diagnoses. Blanket diagnostic statements
included in the files were not considered in these codings. (Such statements were of limited use anyway,
because they predated and thus did not include A-C response). Of course, VN made blanket diagnoses, either
explicitly or implicitly, during the course of treatment. It is quite possible, if not likely, that
classification by the 2 methods could be different for a minority of difficult
to classify patients. Thus, it was
decided, as a secondary measure, to have VN classify each of the 100 patients
as TLD, control, or indeterminate -- mirroring the objective classifications.
For this purpose, JP sent VN a final list of the 100 patient file names
(initials) along with date of birth and gender.
These clinical evaluations were based on VN’s recollections, which were
clearer for some patients than others.
He specifically did not consult the EEG, INSET, SPE, anticonvulsant
responsiveness or etiology data, but did review his overall diagnostic
Final Classifications. After VN completed his clinical
classifications, JP sent his codes to VN.
VN examined these, noting discrepancies with his clinical
classifications. When there were
disagreements, he consulted the files and in most cases agreed with JP. However, there were 8 instances where he
questioned the validity of JPs codings: 2 on EEG and 6 on A-C response. He sent JP relevant excerpts from these files
and JP coded these excerpts blind. Then
VN sent JP the file IDs and JP went back to reassess the basis for his
codings. He did not automatically agree
with his coding of the excerpts, because his original codings had been
influenced by statements in the files other than those selected by VN. He decided to change his codings on 5 of the
6 A-C responses, but not on the other A-C response and on 1 of the EEGs. In the 5 A-C response cases, he found that he
had simply missed statements in the files that, had he been aware of them,
would have affected his original codings.
For the remaining EEG case, VN discovered that there was an error in the
file: the word “not” was erroneously introduced into a statement that should
have read “support” TLD. (This is credible, because a companion statement
immediately below the one in question said that the EEG results support
prescription of anti-convulsant drugs.)
The net result was a reclassification of 5
patients from JP’s original codes: 2 went from control to TLD, 1 went from TLD
to control, 1 went from indeterminate to control, and 1 went from control to
indeterminate. At this point, JP and VN agreed on the classification of 97 of
the 100 patients. 2 remaining patients, who were not among the 7 questioned by
VN earlier, had both been coded as control by JP; 1 was coded indeterminate and
the other TLD by VN. The third (who had
been shifted to the control group by JP) was a difficult patient to code
because of A-C drugs being used for bipolar illness and possible temporal lobe
symptomatology. It was agreed by JP and VN to treat him, like the other 2, as
indeterminate for the test of the hypothesis.
Generation of the SPE scores
involved coding the frequency of the 4 INSET questions for SPEs, using
essentially the same coding as for the INSET questions for TLD:
= 0 (never)
= 1-2 (rare, yearly or
= 3 (occasional, more than
yearly up to monthly, etc.)
3 = 4-6 (frequent, more than monthly, etc.)
We decided to combine the two ESP questions because a few of
the sub-items overlapped and we wanted to avoid double scoring any
experiences. Each of the three remaining
items was scored only once, using the higher of the responses in either the
“recent” or “past” column. This gave a possible range of 0 – 9 for the raw SPE scores.
pre-defined protocol, HN had reviewed the whole chart for SPEs. In three
instances, she had already recorded file notes of SPEs for ESP and presences,
described by patients after taking the INSET.
Because the information
about subjective ESP (S-ESP) experiences obtained from the INSET items was
sketchy, it was decided that JP would interview by phone as many patients as
possible who had reported S-ESP experiences on INSET. ESP experiences were singled out because they
are the most likely kind of SPE to have a true paranormal component. A second
objective of the interviews was to get patients’ impressions of whether they noticed
any effect of the A-C medications they had been taking on the frequency of
their ESP experiences.
In order to protect his
patients, VN excluded from the interviews those with whom he could not discuss
the procedure face-to-face beforehand or whom he felt might be adversely
affected by the interview because of fragility. In one other case, the patient
declined to be interviewed. For these
reasons, only 20 of the 53 patients (37.7%) reporting S-ESP experiences were
designated for interview. However, VN considers them representative of the
larger sample in regard to S-ESP experiences.
Some of the interviews were conducted a considerable period of time
after the original obtaining of the source data, in some instances several
years. 18 of the 20 interviewees were female.
Neppe and Magill attempted
to reach these patients. If they
succeeded, the nature of the phone interview was described to them and informed
consent obtained. JP was given only the
first names of the patients. Because
these were not the same as the patient initials he had been given for the
purpose of coding clinical symptoms, he was effectively blind to how each
patient had been scored on these variables, at least during discussion of the
ESP experiences. The interviews were
tape recorded, with the patients’ consent, and transcribed. None of the patients expressed any
reservations about the taping.
interviews, JP asked the patient to describe their most impressive ESP
experience, in the sense of which they would choose if they were trying to
convince a skeptical friend that ESP is real.
If the chosen experience did not appear to be genuine, JP asked for
another example. They were then asked to
indicate what specific anti-convulsant drugs they had taken during the course
of their treatment and whether they noticed an increase, decrease, or no change
in the frequency of their S-ESP experiences as a function of changes in their
interviews, JP rated on a 3-point scale the quality of the best ESP experience
described by the patient: (a) a “2”
meant that the experience was credible, in the sense that, if it occurred as
described, it was unlikely to be a mere coincidence and there was no prior
information available from which the event could be logically inferred. An
example of an experience in this category is one where the patient had an
impression of a traffic accident which he witnessed 7-minutes later and
included an accurate image of a child going through the car window; (b) a “1”
meant the experience was marginally credible.
An example here is a general statement that the patient often “knew”
that a particular person was about to phone them and that person in fact
promptly called; (c) a “0” meant that the experience was not credible, or the
patient denied having any ESP experiences.
An example here would be a general statement that the patient had
insights into what she had done wrong in her marriage. The effects of A-C drugs
on S-ESP were rated as positive (more SPEs with the change), negative, or none.
SPEs. The mean SPE score was 2.54 (SD =2.46). The distribution shows a pronounced positive
skew. 61% of the sample claimed at least
1 ESP experience, 29% claimed at least 1 OBE, and 35% claimed at least 1
encounter with a presence. The scores of
the 3 questions were moderately intercorrelated, with Spearman correlations
ranging from .345 to .536.
The 16-item INSET was shown to have a high Brown-Spearman odd-even
reliability of .863. The distribution of
classification scores for the 4 components of TLD are presented in Table 1, and
the relationships among them are presented in Table 2.
Although these relationships are generally positive, only the one between EEG
and A-C response is substantial and significant. The size of this effect is due to the fact
that patients not prescribed an A-C medication were coded 0 on A-C Response,
and the decision not to prescribe was heavily influenced by a normal EEG. When these patients are excluded (see last
column of Table 2), the relationship vanishes.
. The 60 patients assigned to the TLD group had a mean
SPE score of 3.05 (SD =2.69). The 27 patients in the control group had a
mean SPE score of 1.93 (SD
=1.90). The difference is marginally
significant by the non-parametric U
–Test (U =1021, p = .049, one-tailed). Thus,
the TLD hypothesis is confirmed. (Recall that the remaining 13 patients were
classified as indeterminate.)
JP noticed during his coding
of symptoms that the patients he was assigning to the TLD group tended to be
female and those he was assigning to the control group tended to be male. This observation was confirmed in the formal
analyses, where it was found that 47 of the 60 females (78.3%) were assigned to
the TLD group and 14 of the 27 males (51.9%) were assigned to the control
group, χ 2 (1, N =
87) = 7.93, p = .005. JP also suspected that females would report
more SPEs than males, and this was confirmed by the data as well. The 60 females had an SPE mean of 3.35,
compared to 1.26 for the 27 males (U
= 1054, p = .005). This, of course, suggests that gender has a
strong potential to confound the TLD-SPE relationship. To assess this, an analysis of covariance was
performed between TLD category and SPE, with gender as a covariate. As expected, the TLD-SPE relationship became
nonsignificant, F (1,84) = 0.91, p = .344. Thus, with gender controlled for, the TLD
hypothesis is not confirmed.
of Component Predictors
To assess the independent
contributions of the components of TLD to the TLD-SPE relationship, these
components (INSET, Etiology, EEG, and A-C Response), plus gender, were treated
as predictors of SPEs in a multiple regression analysis. The analysis was performed on all 100
cases. Only the independent
contributions of gender, t(94) = 2.98
, p = .004, and INSET, t(94) = 4.74, p < .001, were significant.
The multiple r was .568. The standardized regression coefficients, in
descending order, were as follows: INSET (.425), gender (.280), etiology
(.005), EEG (-.008), and A-C response
The INSET clearly has the strongest
relationship with SPEs among the four TLD components and it is significant
independent of gender. It means that the
positive TLD-SPE relationship is completely attributable to the INSET. Gender continues to be an independently significant
predictor of SPEs.
Of the 20 patients interviewed, 13 (65%) received a credibility of score of 2,
5 (22.7%) received a score of 1, and 4 (18.2%) received a score of 0. 2 of the 4 patients who scored 0 contacted VN
privately to the effect that because they didn’t know JP they did not share
with him their best experiences.
In addition, VN made his own
ratings based on his notes and recall about conversations with his patients
about their SPEs. His ratings reflected
SPEs in general more than JP’s, who asked specifically about S-ESP experiences. His initial
ratings were somewhat more positive than JP’s. He gave a rating of 2 to 16
patients (80%), a rating of 1 to 3 patients (15%), and for the remaining 1 he
felt he had too little information to make a rating (5%). On 2 cases where his
codings differed from JP’s, he modified his original codings after consultation
with JP. This made his final ratings as
follows: 2: 14 patients (70%); 1: 5 patients (20%); no rating: 1 patients
(5%). The final ratings are illustrated
in Table 3.
JP interviewed 2
additional patients who, unbeknownst to him at the time, did not report any S-ESP
experiences on the INSET and thus were not among the 53 ESP-positive
patients. He gave both these patients a
rating of 1, and for 1 of these he had been tempted to make it 0.
A-C Drugs. Five patients had not taken A-C drugs and could
not give meaningful responses to the question, and 1 additional patient did not
comply with the request to take the prescribed A-C drugs. Of the remaining 14, 8 (57.1%) claimed to JP
that at least one of the A-C drugs inhibited their ESP experiences, 2 (14.3%)
claimed at least one had a facilitating effect, and 4 (28.6%) claimed no effect
either way. There were no reliable indications
that any specific drug or drugs had a particular kind of effect or no
VN’s initial codings
reflected the trend toward suppression of S-ESP experiences by drugs a bit more
strongly than JP’s. He concluded that A-C drugs had an inhibiting effect on 13
of the 14 relevant patients (92.9%), and no effect on 1 patient (7.1%).
Following consultation with JP on the two cases in which JP coded for a
positive effect of the drug on S-ESP experiences, he modified one of his
ratings. Thus, the final tally for VN was: inhibiting effect, 12 of 14 (85.7%),
no effect, 2 of 14 (14.3%). The ratings are illustrated in Table 3.
The most important finding
to emerge from the data analyses completed so far is the significant positive
relationship between SPE scores and scores on those INSET items scored for
TLD. This outcome confirms the earlier
results of Neppe (1983b), who found that members of the South African SPR who
reported SPEs scored higher on an earlier version of the INSET than those not
reporting SPEs. The only difference is
that in Neppe’s (1983b) study, SPEs were treated as the independent variable
and in the present study the INSET TLD scores were the independent variable.
Thus, findings from a non-clinical population have been confirmed using a
clinical population, namely, that there is a correlation between temporal lobe
symptomatology and subjective paranormal experience.
The finding with INSET
supersedes and to an extent redefines the relationship between TLD and SPEs
that constituted the main hypothesis. It
is noteworthy in this connection that INSET scores did not correlate
significantly with any of the other contributors to the TLD
classification. This pattern of results
suggests that INSET is measuring something not reflected in patients’ EEGs, for
Gender revealed itself to be
confounding factor in the TLD-SPE relationship.
It could be that females have attributes that make them more susceptible
than males to seek out treatment for TLD related symptoms. In any event, our
findings seem to indicate that VN more frequently diagnoses his female patients
as having TLD than his male patients.
It is noteworthy that the gender difference applies to the EEG and
etiology codings, not just the INSET (see bottom of Table 4). Thus, more is at play here than a possible
female bias to report more TLD symptoms or more frequent TLD symptoms than
Even if these findings
reflect a genuine non-artefactual difference of temporal lobe symptoms in a
known group with temporal lobe dysfunction correlating with a higher incidence
of subjective paranormal experiences, the possibility still exists that the
findings reflect a personality predisposition or attitudinal or behavioral
response pattern in this population. This would imply that some people are more
likely to take note of experiences in their lives which they then interpret as
anomalous and that these same people may report experiential symptoms of
temporal lobe anomalies. However, this explanation is unlikely to explain the results
fully, as the specific cluster of symptoms that the patients had are very
uncommon in the general population. (Neppe, 1981a, c; Neppe and Tucker, 1992)
Moreover, the population of patients had diagnosed temporal lobe disease by a
recognized expert in the area (VN), and were being successfully medicated for
this. Nevertheless, the possibility exists that certain temporal lobe
dysfunction patients may be more predisposed to endorsing symptoms, and this
may explain why they may have endorsed more SPEs as well as temporal lobe
symptoms on the INSET. However, these patients had also separately had detailed
personality testing on Minnesota Multiphasic Personality Inventory and other
neuropsychological tests, as well as detailed clinical assessments and neuropsychiatric
evaluations over many sessions. These have not been analyzed as part of the
research, but it is VN's strong clinical impression that there was no
demonstrable personality type or attitudinal predisposition. Even if either of
these explanations exist, this does not rule out the clinically diagnosable
temporal lobe dysfunction.
Overall, JP was reassured
about the general quality of the ESP experiences of the patients he interviewed
over the phone. He was surprised at how
articulate they were, and the great majority seemed to understand what was
necessary if an ESP experience is to be considered credible. Recall that patients with serious psychiatric
problems were removed from the sample at the outset. However, no claim is being made that any of
the experiences can be considered evidence for ESP.
It is clear from these data
that if an A-C drug has a perceived effect on S-ESP experiences, the effect is
most often to reduce their frequency. As
it was found from the original analyses that at least some of these drugs
almost universally helped alleviate patients’ clinical symptoms, this
inhibitory effect on S-ESP suggests that to some degree S-ESP experiences and
the clinical symptoms have a common root.
Limitations of the Study
There are limitations to the
current statistical analysis, all of which may have weakened the obtained
1) In addition to the Short
INSET being used here, VN interviewed the patients in significant detail about
their symptoms, meaning that the TLD side of symptom analysis was more detailed
than the short INSET itself. However, the same cannot be said about the SPE
2) In Neppe's (1983b) original work, extensive
and detailed information was obtained about subjects’ SPEs, and this was used
to select an initial experimental group of "subjective paranormal
experients" that reflected an extreme level of ESP experiences. This extreme group was compared to a control
group with no SPEs. We plan comparable exploratory analyses of the present
data, comparing patients reporting no SPEs versus those reporting large
numbers, based on our revised SPE scores. We will then look for specific
diagnostic factors that distinguish the two groups.
3) Based on clinical
impression, VN feels many of the "SPEs" found in the control group
may not fit a more stringent definition of SPE. This is another reason for a
more detailed evaluation of these SPEs.
4) A late methodological
decision was made to allocate a score of 2 for a handful of subjects in which
frequency of SPEs was not mentioned in the file. Although this was the proper
decision from a research methodology point of view, based on VN's clinical
experience a score of 1 may have been more appropriate for these patients.
5) The EEG scores were based
on surface recordings that did not necessarily register possible deep-seated
pathological temporolimbic activity.
This may explain why some patients with high scores in the other TLD
diagnostic criteria revealed normal EEGs, thus producing a low correlation
between EEG and these other criteria and adversely affecting the predictability
of the SPE scores. Moreover, in the
original Neppe (1980b, 1983b) work on the SASPR population, despite the
subjects having numerous SPEs correlating with possible temporal lobe symptoms,
the EEGs were normal (Nelson and Neppe, 1980).
6) Responsiveness to
medication can be an excellent state-related index of the condition underlying
pharmacological toleration and responsiveness (Neppe, 1990), as well as tracing
underlying biochemical and electrical abnormality including ostensible SPEs and
geomagnetic variations (Neppe, 1999). The correlation between SPE frequency and
anticonvulsant responsiveness may be better measured by tracking the
differences in frequency of SPEs after administration of anticonvulsants, just
as the possible temporal lobe symptoms should also be so tracked. Our present
study instead used a generic score for anti-convulsant response. We plan to
follow up to obtain more longitudinal correlation data.
7) In contrast with the
original Neppe (1980b, 1983b) SASPR study, this study did not distinguish state
and trait temporal lobe phenomena: The study looked at symptoms broadly
occurring over time, without directly correlating state related events. We hope
to clarify this difference in follow-up interviews with the subjects.
This is the first study demonstrating that subjects
with clinical temporal lobe dysfunction demonstrate a strong relationship
between their clinical temporal lobe symptomatology and SPEs. Given the extremely detailed notes that were
reviewed and the care in accurate scoring, it appears to be a real,
non-artefactual statistical result.
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Specific TLD and SPE Items
How often do you have ( ) fits, ( ) seizures or ( ) "peculiar spells”?
How often have you had a ( ) blackout or ( ) lost consciousness for a short
period for no reason?
How often have you had ( ) grand mal or ( ) petit mal or ( ) myoclonic or
( ) psychomotor seizures?
How often do you have or are you told that you at times lose contact
with ( ) staring spells or ( ) absences or ( ) episodes where you have a blank
look on your face ( ) for seconds or ( ) minutes not hours?
How often have you for a very short time like seconds or minutes been completely
unaware that you did or been told that you did any of the following: ( ) odd behaviors like ( ) buttoning /
unbuttoning; ( ) chewing / mouth movements or ( ) other unusual movements or (
) doing very strange things or ( ) saying strange things or ( ) finding
yourself in places you don't remember going to or ( ) jerking the arms?
How often do you ( ) have clear cut gaps
in your memory during which you totally cannot remember anything for 5
minutes or more; ( ) miss major sections of TV shows you have been watching; (
) find yourself driving without remembering how you got there or where you are
going; ( ) do strange things automatically? Include only if you think
these are not only because of difficulty you have concentrating.
How often do your ( ) moods, ( )
feelings or ( ) thoughts fluctuate within minutes for no reason [like
moods which are one moment ( ) very happy then very sad]?
How often do you have odd sensations in part of your body like ( ) floating,
( ) turning or ( ) moving when you were doing none of those?
How often have you come across a smell when there is nothing to cause
it? If so, what kind (check applicable)?
( ) medicine; ( ) steak; ( ) perfume;
( ) flowers;
( ) burning; ( ) rotting; ( ) synthetic; ( ) vomit;
( ) incense; ( ) musty; ( ) grass;
) bitter; ( ) sweet; ( ) cake; ( ) mustard; ( ) other __________ [ONLY “BURNING”,
How often have you seen any of the following when there is no-one or
nothing to cause it? ( ) dots; ( ) lights;
( ) patterns; ( ) shapes; ( ) wrong size; ( ) movements;
( ) distortions; ( ) things moving; (( )
stars; ( ) bugs; ( ) threads;
( ) insects; ( ) none;
( ) other ___________________ [ONLY “MOVEMENTS”, “DISTORTIONS”, “WRONG SIZE”
How often do you hear any of the following, when there is no-one or
nothing to cause it? ( ) buzz;
( ) ring; ( ) sizz; ( ) hiss;
( ) tap; ( ) songs; ( ) whistling; ( ) music;
( ) single word; ( ) arguing; ( )
names; ( ) voices;
( ) jumble; ( )
( ) instructing; ( )
radio / TV; ( ) phone; ( )
nothing; () other __________ [ONLY
“BUZZ”, “RING”, “HISS”, “TAP” SCORED]
How often have you been in a familiar place and had the impression that you
have never been in that place before? (the opposite of déjà vu called
jamais vu - not recognized at all, totally unfamiliar)
How often have you found that, for no apparent reason, you are actually
reliving things in the past (as if the past flows like a movie screen
How often do you have sudden, unexplained and uncontrollable attacks of intense
How often do you hear what is being said, yet you cannot understand or
make sense of it?
How often do you have frightening nightmares?
How often have you had ( ) premonitions or ( ) "psychic", ( )
( ) paranormal experiences such as ( )
knowing the future , ( ) sensing correctly unknown past knowledge , ( ) having dreams which came true, or ( )
strange feelings which came true?
50) How often have you felt you’ve ( ) seen
events that happened at a great distance before or while they were happening or
( ) been in touch with someone when they were far away from you or dead?
How often have you felt you have ( )
left your body or ( ) had an out of body
How often have you been aware of a presence of someone whom you could not see?
Frequencies of Diagnostic
0 1 2 3
INSET 9 32 18 41
ETIOLOGY 47 44 9
EEG 28 14 24 34
A-C RESPONSE 23 a 16 36 25
a Includes 1 score of –1.
Predictors Expressed as
INSET ETIO. EEG A-C
RSP. A-C RSP (2)a
INSET .080 .120 .110 -.083
ETIOLOGY .081 -.011 -.057
SEX .285** -.198 .252* .148 -.050
aOnly patients who were prescribed an A-C medication,
N = 80.
*** p <
.001; ** p < .01; * p < .05
Final Ratings on Phone Interview Questions
QUALITY OF S-ESP EFFECT OF DRUGS
JP VN JP VN
Score N N Effect N N
2 13 14 Neg. 8 12
1 4 5 None 4 2
0 3a 0 Pos. 2 0
N/Rb 0 1 N/Rb 0 0
Total 20 20 Total 14 14
aIncludes 2 patients who told
VN they under-reported
S-ESP experiences to JP
bN/R means not rated.