A controlled analysis of subjective paranormal experiences in temporal lobe dysfunction in a neuropsychiatric population

John Palmer

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 (Seattle, WA). TLD was defined as a composite of 4 diagnostic criteria: (a) symptomatology as measured by 16 TLD items from Neppe's INSET questionnaire; (b) predisposing conditions (recreational drugs, brain damage); (c) anomalous electroencephalographic activity; and (d) response to anticonvulsant 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 who were each sent portions of patient files from which information relevant to the other rater had been removed. Sixty patients classified as having TLD had significantly more SPEs than 27 patients who were not. Thirteen patients indeterminate on T LD were removed. Supplementary regression analyses revealed that this result was due entirely to symptoms (INSET) as predictor. 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 most had at least 1 credible ESP experience.

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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 the 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 subjective paranormal experiences (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 electroencephalographic (EEG) readings. Subsequently, Nelson and Neppe (1980) failed to 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 epileptic.

The first controlled study to investigate the relationship between temporal lobe instability and SPEs was by Neppe (1979, 1980, 1981b, 1982, 1983d), 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 prestipulated criteria. These persons had significantly more possible temporal lobe symptoms than a group of six control members 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 participants 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 experiences.

Neppe later delineated a particular type of olfactory hallucination associated with SPEs that is pleasant and perfumy but commonly coexists with temporal lobe type hallucinations (Neppe, 1983a, 1983b). 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 participant each describe a specific subtype of deja vu experience (Neppe, 1981b, 1983c).

Persinger has published extensive research and theorizing on the role of the temporal lobes in psi experiences. He attributes SPEs to instability or microseizures 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, 1981b, 1981c). 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 in addition to the scale used previously (Persinger & Vaillant, 1985). Both scales yielded sign ificant 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 & Broughton, 2000).

Persinger's temporal lobe 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 & Persinger, 1990). However, the scales do not show particularly good discriminant validity as measures of temporal lobe epilepsy. Clinical groups suffering from posttraumatic 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 of 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) argued that repeated epileptic motor seizures destroy brain tissue and thus might actually reduce the incidence of SPEs. Sensky, Wilson, Petty, Fenwick, and Rose (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 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-ge netics" (Neppe & Hurst, 1982). Clearly, more research is needed to settle the issue.

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 (PNI) in Seattle, Washington. He collects enormous amounts of data from each individual, including etiology, current symptoms, EEG data, and responses to anticonvulsant (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, 1981a, 1981b, 1981c) and later by Neppe and Tucker (1988, 1992).

Although it is Neppe's subjective impression that his temporal lobe dysfunction (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.

METHOD

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. John Palmer (JP) and Vernon 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. Of these, 8 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 of the patients included in the sample gave informed consent to have their files used for the research. Only 6 qualifying patients 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 January 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 EEC data during the evaluation or in the preceding 6 months). Approximately 15 to 20 cases were excluded by these criteria.

Preparation of Computer Files

At the outset, to preserve anonymity, the names of patients were converted to their initials plus a digit. (1) 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 Heidi 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 temporal lobe and seizure symptoms was removed from the files sent to HN. (2) All this editing, including the removal of patient names, was done by HN for the 82 patients and by Stacie Magill (SM) for the last 18 patients. (3) 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 Microsoft 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.

Diagnostic Information

There were four specific classes of diagnostic information that the raters used to assess whether patients were to be assigned to the temporal lobe group or to the control group. They are described briefly below.

Short INSET. The Short form of the 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 seven response choices representing frequency of occurrence: 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, 16 refer to symptoms that VN has found to be strongly characteristic of TLD based on his extensive clinical experience. 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, and apparitions. These questions, which provided the SPE scores, are listed at the bottom of the Appendix.

Patients completed the INSET during their first or second visit to PNI. After completing it, they were interviewed by VN 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 (hereinafter referred to simply as the INSET).

Etiology. 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 electroence-phalographically. Depending on clinical indications, they receive either or both of:

1. Eighteen-channel wake and sleep EEGs including activation procedures of hyperventilation and photic stimulation.

2. Two 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, pushbutton 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-wa ve 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 arrhythmias.

All but 7 of the 100 patients in our sample were given the ambulatory EEC. In 6 of these cases the exclusion was because the sleeping and waking EEGs were both normal and there were no other reasons to think the ambulatory EEG might yield a different verdict. In 1 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 subsection 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 EEC was appropriate. In these cases, the reports of these earlier EEGs were considered for the coding.

Response to A-C medications. If the previously obtained diagnostic information indicates that the patient is experiencing seizures or is likely to have TLD, they are generally given one of a variety of A-C 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 medication 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 antidepressants or antianx iety agents, in addition to the A-Cs.

Diagnostic Coding

At the 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 scores.

TLD symptoms (0 to 3). The frequency scores on the 16 INSET items devoted to TLD were transformed as follows:

0 = 0 (never)

0.25 = 1-2 (rare, yearly or less, etc.)

0.50 = 3 (occasional, more than yearly up to monthly, etc.)

1 = 4-6 (frequent, more than monthly, etc.)

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 O 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

Etiology (0 to 2). One 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, or amnesia.

One 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 EEC reports generally contained information about the number of spikes and paroxysms in the EEC 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 support" TLD

2 = "abnormal"; "support" or "moderately support" TLD

3 = "severely abnormal"; "strongly support" TLD

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 EEC abnormalities recorded in each file, eliminated any phrases that might identify the patient (e.g., name of physician who had conducted previous EEC 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 sent. (4)

A-C response (-3 to 3). The response of patients' symptoms to A-C medications was coded on a 7-point scale from -3 (much worse) to 3 (much better). 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 A-C drug.

Patients for whom no A-C drug was recommended or 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.

TLD Classification

Objective classifications. The classification scores were summed over the four diagnostic categories (symptoms, etiology, EEC, and 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: TLD group

-3 to 4: control group

5: indeterminate

The indeterminate group was decided on 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 a relatively 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 two 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 EEC, INSET, SPE, A-C responsiveness, or etiology data but did review his overall diagnostic assessment. (5)

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 in which he questioned the validity of JP's 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 6A-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, V N 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 EEC results support prescription of A-C 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. Two 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 3rd (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. JP and VN agreed to treat him, like the other 2 patients, as indeterminate for the test of the hypothesis.

SPE Scores

Generation of the SPE scores involved coding the frequency of the four INSET questions for SPEs, using essentially the same coding as for the INSET questions for TLD:

0 = 0 (never)

1 = 1-2 (rare, yearly or less, etc.)

2 = 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 subitems 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.

Per predefined 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.

Phone Interviews

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.

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. Eighteen of the 20 interviewees were female.

VN and SM 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.

During the interviews, JP asked the patients 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. The patients were then asked to indicate what specific A-C 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 drug regimen.

Following the interviews, JP rated on a 3-point scale the quality of the best ESP experience described by the patient:

* 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 in which the patient had an impression of a traffic accident that he witnessed 7 mm later and included an accurate image of a child going through the car window.

* 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.

* 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.

RESULTS (6)

Scores

* SPEs. The mean SPE score was 2.54 (SD = 2.46) on the 0 to 9 scale. The distribution shows a pronounced positive skew. Of the sample, 61% claimed at least one ESP experience, 29% claimed at least one out-of-body experience, and 35% claimed at least one encounter with a presence. The scores of the three questions were moderately intercorrelated, with Spearman correlations ranging from .345 to .536.

TLD components. The 16-item INSET was shown to have a high split-half reliability of .863. The distribution of classification scores for the four components of TLD are presented in Table 1, and the relationships among them are presented in Table 2. (7) 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.

TLD Hypothesis

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 nonparametric Mann-Whitney U test (U = 1,021, p = .049, one-tailed). Thus, the TLD hypothesis is confirmed. (Recall that the remaining 13 patients were classified as indeterminate.)

Gender

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 female patients (78.3%) were assigned to the TLD group and 14 of the 27 male patients (51.9%) were assigned to the control group, [chi square](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 a mean SPE score of 3.35, compared with 1.26 for the 27 males (U = 1,054, p = .005). This, of course, suggests that gender has a strong potential to confound the TLD-SPE relationship. To assess this, we performed an analysis of covariance 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 confirm ed.

Analysis of Component Predictors

To assess the independent contributions of the components of TLD to the TLD-SPE relationship, we treated these components (INSET, etiology, EEC, and A-C response), plus gender, as predictors of SPEs in a multiple regression analysis. (8) 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 (-.153).

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.

Phone Interviews

S-ESP. Of the 20 patients interviewed, 13 (65%) received a credibility score of 2, 5 (22.7%) received a score of 1, and 4 (18.2%) received a score of 0. Two of the 4 patients who scored 0 contacted VN privately to the effect that because they did not 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 in which his codings differed from JP's, he modified his original codings after consultation with JP. This made his final ratings as follows: a rating of 2 for 14 patients (70%); a rating of 1 for 5 patients (20%); and no rating for 1 patient (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 effect.

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 2 cases in which JP coded for a positive effect of the drug on S-ESP experiences, VN modified one of his ratings. Thus, the final tally forVN was: inhibiting effect, 12 of 14 (85.7%); no effect, 2 of 14 (14.3%). The ratings are illustrated in Table 3.

DISCUSSION

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 (1983d), who found that members of the SASPR 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 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 nonclinical population have been confirmed using a clinical population, namely, that there is a correlation between temporal lobe symptomatology and SPE.

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 example.

Gender revealed itself to be a confounding factor in the TLD-SPE relationship, as females reported both more TLD symptoms and more SPEs than males. The tendency for females to report more SPEs than males has been found in survey data (e.g., Haraldsson & Houtkooper, 1991; Schouten, 1981), but it is not clear if this result is due to response biases or genuine differences in prevalence of SPEs (Palmer & Neppe, 2002). In the present case, 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 codings, not just the INSET (see bottom of Table 2). Thus, more is at play here than a possible female bias to report more TLD symptoms or more frequent TLD symptoms than males.

Even if these findings reflect a genuine nonartefactual difference of temporal lobe symptoms in a known group with TLD correlating with a higher incidence of SPEs, 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, 1981b; Neppe & 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. These patients also received detailed personality testing on the 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.

Nevertheless, the possibility exists that certain TLD 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. One way to resolve this issue is to look at how they answered other questions on the INSET that were not considered strongly characteristic of TLD. We plan to examine these other items in follow-up research. Even if such response bias problems exist, this does not rule out clinically diagnosable TLD.

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 Wan 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 present statistical analysis, all of which may have weakened the obtained results.

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 analysis.

2. In Neppe's (1983d) original work, extensive and detailed information was obtained about participants' 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 with a control group with no SPEs. We have conducted comparable exploratory analyses of the present data, comparing patients reporting no SPEs versus those reporting large numbers, based on our revised SPE scores (Palmer & Neppe, 2002). We found 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 an SPE score of 2 for a handful of participants in which prevalence 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 EEC and these other criteria and adversely affecting the predictability of the SPE scores. Moreover in the original Neppe (1980, 1983d) work on the SASPR population, despite the participants having numerous SPEs correlating with possible temporal lobe symptoms, the EEGs were normal (Nelson & 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 A-C responsiveness may be better measured by tracking the differences in frequency of SPEs after administration of A-Cs, just as the possible temporal lobe symptoms should also be so tracked. Our present study instead used a generic score for A-C response. We plan to follow up to obtain more longitudinal correlation data.

A-Cs are now being used in other contexts such as mood disorder stabilization, neuropathy, and headaches. This may complicate interpretation in a general psychiatric or neurological population of why responses occur. However, this is less so in a seizure/spell-type population, where for the past centuty A-C responsiveness has been a standard measure of efficacy of these drugs in epilepsy.

7. In contrast with the original Neppe (1980, 1983d) 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 participants.

CONCLUSION

This is the first study demonstrating that patients with clinical TLD demonstrate a strong relationship between their clinical temporal lobe symptomatology and SPEs. However, the SPE reports and the scores on the clinical symptom list did not correlate with EEG findings of TLD. This lack of correlation may initially appear surprising, but it should be kept in mind that the LEG scores are based on surface recordings that did not necessarily register possible deep-seated pathological temporolimbic activity. VN believes TLD diagnostic criteria in a neuropsychiatric population frequently reveal normal EEGs, despite these sometimes extremely complicated, refractory or previously nonresponsive patients responding to A-C medication.

APPENDIX

TLD and SPE Items From the Inventory of Neppe of Symptoms of Epilepsy and the Temporal Lobe (INSET)

Temporal Lobe Dysfunction (TLD) Items

(1.) How often do you have () fits, () seizures or () "peculiar spells"?

(2.) How often have you had a () blackout or () lost consciousness for a short period for no reason?

(3.) How often have you had () grand mal or () petit mal or () myoclonic or () psychomotor seizures?

(4.) 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?

(6.) 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?

(7.) 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.

(8.) 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]?

(11.) How often do you have odd sensations in part of your body like () floating, () turning, or () moving when you were doing none of those?

(12.) 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," "ROTTING" SCORED]

(13.) 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" SCORED]

(15.) 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; ( ) jumbe; ( ) message; ( ) instructing; ( ) radio / TV; ( ) phone; ( ) nothing; ( ) other _____ [ONLY "BUZZ," "RING," "HISS," "TAP" SCORED]

(19.) 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 deja vu called jamais vu--not recognized at all, totally unfamiliar)

(23.) 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 before you)?

(28.) How often do you have sudden, unexplained, and uncontrollable attacks of intense fear?

(34.) How often do you hear what is being said, yet you cannot understand or make sense of it?

(48.) How often do you have frightening nightmares?

Subjective Paranormal Experience (SPE) Items

(49.) How often have you had ( ) premonitions or ( ) "psychic," ( )intuitive or ( ) 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?

(51.) How often have you felt you have ( ) left your body or ( ) had an out of body experience?

(52.) How often have you been aware of a presence of someone whom you could not see?

TABLE 1

FREQUENCIES OF DIAGNOSTIC CODES

Variable       0       1   2  3

INSET          9      32  18  41
Etiology      47      44   9  NA
EEG           28      14  24  34
A-C response  23 (a)  16  36  25

Note. INSET = Inventory of Neppe of Symptoms of Epilepsy and the
Temporal Lobe;

EEG = electroencephalographic data;

NA = not applicable;

A-C = anticonvulsant.

(a) Includes one score of -1.

TABLE 2

RELATIONSHIPS AMONG PREDICTORS EXPRESSED AS SPEARMAN CORRELATION
COEFFICIENTS

Variable        1        2       3      A-C Rsp.    A-C Rsp. (2) (a)

1. INSET        -      .080    .120       .110         -.083
2. Etiology              -     .081      -.011         -.057
3. EEG                           -        .361 ***      .000
Sex          .285 **  -.198    .252 *     .148         -.050

Note. A-C Rsp. = anticonvulsant response; INSET = Inventory of Neppe of
Symptoms of Epilepsy and the Temporal Lobe;

EEG = electroencephalographic data.

(a) Only patients who were prescribed an A-C medication, N=80.

* p<.05.

** p<.01.

*** p<.001.

TABLE 3

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              3 (a)      0        Pos.          2         0
N/R            0          1        N/R           0         0
Total         20         20       Total         14        14

Note. S-ESP = subjective ESP; JP = John Palmer; VN = Vernon Neppe; Neg.
= negative; Pos. = positive; N/R = not rated.

(a)Includes 2 patients who told VN they underreported S-ESP experiences
to JP.

(1.) All names were changed to initials and numbers (first in the series, 1 and if a duplicate initial, 2, then 3, etc.).

(2.) To create profiles for SPE ranking (for HN),all INSET questions not pertaining to SPE, deja vu, or presences, plus any temporal lobe terminology, seizure terminology, and diagnosis information, were extracted. For the ranking of temporal lobe symptomatology (for JP), all information about SPEs, ESP, PK, intuition, presences, deja vu, out-of-body experiences, and auras was extracted, leaving all temporal lobe and diagnostic information.

(3.) At the time of the editing, both HN and SM were employees of the Pacific Neuropsychiatric Institute. SM took over the duties from HN when SM was added to the staff. JP was appointed an honorary staff member prior to the start of the study.

(4.) JP attempted his own codings of these cases before mailing them to VN. His codings matched VN's in 10 of the 16 cases. In 5 of these misses, JP was one number too low; in the 6th, he was one number too high. The final TLD classifications of these 6 patients would not be changed had JP's codings been used.

(5.) VN spontaneously recalled more than 90 of the patients in detail. Those that he did not were generally patients who had not consulted him for a year or more and whose case histories had not required review during that time.

(6.) All p values are two-tailed unless noted otherwise.

(7.) Prior to analysis, subgroups of less than 10 were combined with an adjacent group.

(8.) The regression analysis was performed on a Spearman correlation matrix.

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Rhine Research Center

2741 Campus Walk Ave., Bldg. 500

Durham, NC 27705, USA

john@rhine.org

Pacific Neuropsychiatric Institute

10330 Meridian Ave. N, Suite 380

Seattle, WA 98133, USA

psyche@pni.org

We are greateful to the Bial Foundation for supporting this research and to Heidi Nebel and Stacie Magill for their assistance in conducting the study. An earlier version of this paper was presented at the 2001 Parapsychological Association Convention. The present paper was peer reviewed under the auspices of Dr. Richard Broughton.

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