Psychopharmacology (2009) 206:563–573
DOI 10.1007/s00213-009-1564-x
ORIGINAL INVESTIGATION
Superstitious conditioning as a model of delusion formation
following chronic but not acute ketamine in humans
Tom P. Freeman & Celia J. A. Morgan &
Elissa Klaassen & Ravi K. Das & Ana Stefanovic &
Brigitta Brandner & H. Valerie Curran
Received: 28 February 2009 / Accepted: 30 April 2009 / Published online: 13 May 2009
# Springer-Verlag 2009
Abstract
Background Ketamine has previously been shown to
induce delusion-like or referential beliefs, both acutely in
healthy volunteers and naturalistically among nonintoxi-
cated users of the drug. Delusions are theoretically under-
pinned by increased superstitious conditioning or the
erroneous reinforcement of random events.
Materials and methods Using a novel and objectively
measured superstitious conditioning task, experiment 1
assessed healthy volunteers before and during placebo (n=
16), low-dose (n=15), and high-dose ketamine (n=16) under
randomized and double-blind conditions. Experiment 2 used
the same task to compare ketamine users (n=18), polydrug
controls (n=19), and nondrug-using controls (n=17).
Results In experiment 1, ketamine produced dose-dependent
psychotomimetic effects but did not cause changes in
superstitious conditioning. Experiment 2 found increased
levels of superstitious conditioning among ketamine users
compared to polydrug and nondrug-using controls, respec-
tively, as evidenced by both objective task responses and
subjective beliefs following the task.
Conclusions Results indicate that chronic but not acute
exposure to ketamine may increase the propensity to adopt
superstitious conditioning. These findings are discussed in
terms of acute and chronic ketamine models of delusion-
like belief formation in schizophrenia.
T. P. Freeman (*) : C. J. A. Morgan : E. Klaassen : R. K. Das :
A. Stefanovic : B. Brandner : H. V. Curran
Clinical Psychopharmacology Unit, Clinical Health Psychology,
University College London,
Gower St,
London WC1E 6BT, UK
e-mail: tom.freeman@ucl.ac.uk
Keywords Dopamine . Glutamate . Schizophrenia .
Modeling . Drug abuse
Introduction
Acutely, the noncompetitive NMDA-receptor antagonist
ketamine induces a range of cognitive impairments and
psychotic-like symptoms in healthy volunteers, including
delusion-like and referential beliefs (Bowdle et al. 1998;
Lahti et al. 2001; Pomarol-Clotet et al. 2006). Recently, it
has been suggested that acute ketamine may provide a
pharmacological model of delusion formation (Corlett et al.
2007; Pomarol-Clotet et al. 2006). Corlett et al. (2006)
employed an associative learning task aiming to link
delusion formation to mismatches between actual and
expected outcomes or “prediction error” signals on an
associative learning task. Compared to placebo, a low dose
of ketamine increased right lateral prefrontal activation
responses to expected contingencies and decreased in
response to mismatches; this was interpreted as a disruption
in prediction error signaling. Further, these frontal
responses were predictive of clinician rated delusion-like
referential beliefs on the Present State Examination.
In chronic recreational users of ketamine, a range of
cognitive impairments and psychotic-like symptoms have
been observed (Curran and Monaghan 2001; Curran and
Morgan 2000; Morgan et al. 2004). We have recently found
evidence of elevated delusional symptoms among recrea-
tional ketamine users when they were not intoxicated with
the drug (Morgan et al. 2009; Uhlhaas et al. 2007). Morgan
et al. found an apparent dose–response effect whereby
frequent users scored higher than infrequent, ex users, and
nonusers, respectively. Further in the frequent users,
delusional symptoms correlated with the amount of ket-
564
amine currently being used. This group also rated greater
conviction in and more preoccupation with their delusions
than all other groups.
Given that delusions have been observed in humans
following both a single dose and repeated exposure to
ketamine, we decided to investigate the effects of both
acute and chronic ketamine on the same assessments of
delusional thinking. Further, as previous studies of
ketamine-induced delusion-like beliefs have used either
clinician or participant ratings, we designed a novel,
objective task aimed at assessing delusion formation, based
on the process of superstitious conditioning.
Superstitious conditioning is a form of associative
learning first documented by Skinner (1948). Skinner
exposed pigeons to a food reward at regular response-
independent intervals and under the principles of operant
conditioning, any behavior a pigeon happened to be
engaged in at the time the reward was delivered would
become positively reinforced. Accordingly, Skinner ob-
served the pigeons adopting a number of strange behaviors,
including head twisting and turning on the spot. These
behaviors are analogous to superstitious behavior in
humans; if a gambler wears a pair of socks on the night
of a big win, these socks might be worn again in the belief
that they are “lucky” when in fact, they were randomly
contingent on reward, just like the movements shown by
Skinner’s pigeons. Similarly, delusions are characterized by
beliefs that defy a cause–effect relationship and may lie
upon the same continuum as superstitious beliefs; as such
superstitious conditioning may provide an analog of
delusion formation (Brugger et al. 1994).
Superstitious conditioning is thought to underpin delu-
sion formation due to chaotic firing in the mesolimbic
dopamine system (King et al. 1984; Shaner 1999).
However, previous demonstrations of superstitious condi-
tioning in humans have not addressed either delusions or
pharmacological models of psychopathology (Aeschleman
et al. 2003; Bloom et al. 2007; Matute 1994; Ono 1987;
Rudski 2001). The aim of this study was to assess
superstitious conditioning following acute and chronic
exposure to ketamine objectively using a novel supersti-
tious conditioning task.
Method
Experiment 1: acute effects of ketamine
Design and participants A randomized double-blind inde-
pendent group design was used to compare a low dose of
ketamine (target plasma level—75 ng/ml) and a high dose
of ketamine (target plasma level—150 ng/ml) with placebo
(saline). Groups were balanced for gender. Healthy volun-
Psychopharmacology (2009) 206:563–573
teers aged 18–35 years were recruited through an adver-
tisement and were paid for participation. All were native
English speakers with no history of (a) serious medical
conditions, (b) personal or family mental health diagnosis,
and (c) substance misuse. The study was approved by the
UCL/UCLH ethics committee, and all participants provided
written informed consent.
All participants attended a screening session (screening
questionnaires, blood pressure, height, and weight) prior to
the experimental session. Of the 58 volunteers meeting the
inclusion criteria, ten dropped out due to adverse effects at
the high dose. Forty-eight volunteers successfully complet-
ed the testing session; however, due to a computer error,
data were not analyzed for one participant in the low-dose
ketamine group. During screening, participants were
assessed on The National Adult Reading Test (NART;
Nelson 1982), a full version of the Brief Psychiatric Rating
Scale (BPRS; Overall and Gorham 1962) and the shortened
Oxford–Liverpool Inventory of Feelings and Experiences
questionnaire (O-LIFE; Mason et al. 2005). Self-reported
abstinence from recent drug use was verified with urinal-
ysis. Participants were required (1) to abstain from the use
of alcohol for 24 h prior to the testing session and (2) to fast
for morning testing from midnight, or for afternoon testing
for >6 h beforehand.
Drug administration Two 20-gauge intravenous cannulae
were inserted into participants’ forearms before predrug
testing (one for the infusion and the other for blood samples),
and 1 l of Hartmann’s solution (Baxter, UK) was administered
over 2 h. Inserting cannulae and administering fluids early
helped with tolerability of ketamine. Ketamine administration
was via a Graseby intravenous infusion pump controlled by
the Stan-pump program (Schafer et al. 1990). The program
used a bolus-elimination-transfer infusion scheme based on
the Clements pharmacological model (Clements and Nimmo
1981). Steady state of predicted plasma ketamine/placebo
concentration according to the model was achieved over a
period of 12 min.
At the beginning of the study, participants received
ketamine (100 or 200 ng/ml) or saline placebo (0.9% NaCl
solution). However, due to dropouts, the dosage was modified
to 75 and 150 ng/ml. This resulted in one participant on
100 ng/ml and two participants on 200 ng/ml being included
in the low- and high-dose groups in the final analysis,
respectively; the remaining participants were tested on 75/
150 ng/ml. Peripheral venous blood samples were taken at 6
and 45 min after achieving the steady state to determine
ketamine concentration in the blood (all blood samples were
from the 75/150 ng/ml groups). Plasma was obtained
immediately by centrifugation and stored at −80°C. Ketamine
levels were measured using gas chromatography (C3P
Analysis Lab, Plymouth, UK).
Psychopharmacology (2009) 206:563–573
Assessments
Superstitious conditioning task
Experimental phase: the experimental phase (see Fig. 1)
was a 108-trial choice task which employed a response-
independent reward contingency. Following a central
fixation cross shown for 1,000 ms, one of the three possible
stimuli appeared to the left of the cross, and two (of the
same three possible) stimuli appeared above and below a
question mark, to the right of the cross. Participants chose,
through trial and error learning, the stimulus on the right
they believed formed the pair with the stimulus on the left
likely to result in the highest number of points. Pairs could
be formed using identical and nonidentical stimuli, in two
possible locations, giving a total of nine possible stimulus
pairs in each version of the task. Two versions of the task
were completed (pre- and post-infusion), each consisting of
different stimuli (yellow, blue, and red stars in version 1,
and red triangles, circles, and squares in version 2). The
order of completion of the two task versions was counter-
balanced between participants.
Following each response, feedback was provided, which
showed the chosen stimulus pair and the amount of points
awarded. In order to prevent excessive salience being
attributed to rewarded versus nonrewarded pairs and to
obtain a continuous measure of superstitious conditioning,
every pair was rewarded equally over the course of the task,
ranging from 20 to 100 points in 20-point intervals. Each
level of points awarded was accompanied by a distinct
“ching” cash register sound: 20 points was accompanied by
one “ching,” 40 points by two “chings,” and so on, with the
amplitude of the sound also increasing in intensity according
to the number of points rewarded. Responses were recorded
in terms of the frequency with which each stimulus pair was
chosen. Practice was given pre-infusion using a “demonstra-
tion version,” in which pairs were chosen from three
different stimuli (flower cartoons). Following five practice
trials with the demonstration version, participants began the
learning phase. Superstitious conditioning was indexed by
the frequency of pair choice. Choices were ranked for
frequency and due to limited spread in the data, superstitious
conditioning was computed as the frequency of most chosen
pair minus frequency of least chosen pair. Ranges were
calculated for individual blocks and over all trials.
Response
Fixation Stimuli Feedback
+ + ? +
1000 ms 1000 ms 20 Points!
Fig. 1 Trial sequence of the experimental phase (version 1) in the
superstitious conditioning task
565
Questionnaire phase To index subjective delusion-like
beliefs formed during the task, participants were given a
post-task questionnaire asking: “in the first part of the task—
where you were given points—did you notice any patterns?”
Participants were given the following answers to choose from:
“yes,” “no,” “not sure,” or “no, they were there but I didn’t
find them.” Participants who responded “yes” to this question
were asked to describe the nature of the “patterns” they had
noticed.
Subjective effects (pre- and during infusion)
The psychomimetic states inventory (PSI; Mason et al.
2008) assesses state schizotypy induced by psychotomi-
metic drugs. The PSI contains 48 alternative forced choice
questions ranging in agreement from 0 (not at all) to 3
(strongly) and has subscales of delusory thinking, perceptual
distortions, cognitive disorganization, anhedonia, mania, and
paranoia. Participants were assessed on three key positive
and four key negative items of the BPRS (see Krystal et al.
1994), yielding scores for positive symptoms, negative
symptoms, anxious depression, and activation.
Procedure After cannulation on the testing day, baseline
blood pressure and heart rate measures were taken followed
by pre-infusion tasks (PSI, key BPRS items, superstitious
conditioning task) and then the start of the infusion. After
the target plasma concentration was theoretically achieved,
post-drug testing commenced (PSI, key BPRS items,
superstitious conditioning task). In addition to the reported
battery of tests, participants also completed two semantic
priming tasks, the results of which are reported in
Stefanovic et al. (2009). After testing, participants were
provided with refreshments and discharged when “street
ready.”
Experiment 2: Chronic self-administered ketamine
Design and participants An independent group design was
used to compare (1) ketamine users who reported using
ketamine more than twice a month for at least 6 months, (2)
polydrug controls, reporting regular drug use other than
ketamine (e.g., ecstasy, amphetamine, cocaine, cannabis) but
who were either ketamine naïve or who had not used ketamine
more than three times in their life, (3) nondrug-using controls
who reported to have never used illicit drugs. Participants
were recruited using snowball sampling (Solowij et al. 1992).
Inclusion criteria were English as a first language and normal
or corrected to normal sight. Exclusion criteria were a family
or personal history of mental health problems or drug
dependence. The study was approved by the UCL Graduate
566 Psychopharmacology (2009) 206:563–573

School ethics committee. All participants provided written onal contrasts compared (1) ketamine groups with placebo
informed consent. and (2) high-dose with low-dose ketamine (experiment 1);
(1) drug users with nondrug-using controls and (2) ket-
Assessments amine users with polydrug controls (experiment 2).

Self-ratings Participants were assessed on trait schizotypy

(shortened O-LIFE; Mason et al. 2005), and on the “spot
the word task” as a correlate of premorbid verbal IQ
(Baddeley et al. 1993).
Superstitious conditioning task The task used was identical
to that described in experiment 1 (version 2).
Procedure Participants were tested in a quiet room at their
own homes. Written, witnessed informed consent was
obtained before testing. A semistructured interview was
carried out concerning participants’ psychiatric history and
lifetime drug use in order to meet inclusion criteria, and
urinalysis was used to confirm that reports of recent drug
use were accurate. Participants were then given the “spot
the word” task, followed by the superstitious conditioning
task (training, learning phase, and questionnaire phase).
Finally, they completed the O-LIFE. Participants also
completed two semantic priming tasks, reported elsewhere
(Stefanovic et al. 2009).
Results
Experiment 1: acute effects of ketamine
Demographics (Table 1) Groups did not differ in age,
gender, NART, O-LIFE, or BPRS scores.
Plasma ketamine levels Mean ketamine plasma concen-
trations were 39.37±23.89 ng/ml in the low dose and
115.08±54.72 ng/ml in the high-dose groups 6 min after
the steady state was achieved; at 45 min, they were 54.64±
17.57 ng/ml (low dose) and 143.42±60.67 ng/ml (high
dose). Norketamine plasma concentrations at 6 min were
4.2±6.32 ng/ml (low dose) and 12.17±9.85 ng/ml (high
dose); at 45 min, they were 22.24±8.99 ng/ml (low dose)
and 50.5±32.62 (high dose).
Superstitious conditioning task

Statistical analyses All analyses were performed using
Statistical Package for Social Sciences (SPPS Version
11.5). Group differences in the experimental phase of the
superstitious conditioning tasks were examined using one-
way ANOVAs (Kruskall–Wallis tests where data were
nonparametric) and RMANOVAs. If transformations did
not yield homogenous variance, RMANOVAs were con-
ducted using nonparametric data. Bonferroni post hoc tests
and Bonferroni-corrected Mann–Whitney U tests were used
to explore simple effects where a significant effect of group
was revealed. Chi-squared tests were also used to explore
dichotomous data. Bonferroni-corrected Pearson correla-
tional analyses were conducted between ketamine use, trait
schizotypy, and superstitious conditioning. Planned orthog-
Data from the superstitious conditioning task were missing
for one participant in the low-dose ketamine group;
therefore, analysis of this task was completed on n=15 in
this group and n=16 in the other two groups.
Experimental phase (Table 2) The experimental phase of
the task was examined in terms of the frequency with which
each of the nine pairs was chosen in each of the three
blocks of trials. The range between the most and least
frequently chosen pairs was used to index superstitious
conditioning, with a high range indicating a high level of
superstitious conditioning. A 3×3×2×2 RMANOVA was
performed with Block (1, 2, and 3 ) and Time (pre- and
post-infusion) as within subjects factors and Group (place-

Table 1 Group means (SD) of

participants’ demographic data Placebo Low dose High dose Group main effect
in experiment 1
Age 24.71 (4.47) 23.10 (3.18) 25.65 (4.29) NS
Gender (N male/female) 8:8 8:8 8:8 NS
NART 113.38 (5.24) 112.19 (4.13) 115.06 (4.42) NS
BPRS 27.56 (2.39) 28.50 (3.01) 26.69 (1.92) NS
O-LIFE (total) 10.25 (5.15) 7.38 (5.14) 9.00 (6.43) NS
Unusual experiences 2.31 (2.09) 1.06 (1.69) 2.31 (2.18) NS
Cognitive disorganization 4.19 (2.51) 3.12 (2.47) 3.13 (2.83) NS
Impulsive nonconformity 2.63 (2.00) 2.06 (1.53) 2.69 (1.85) NS
Introvertive anhedonia 1.13 (1.41) 1.13 (1.26) 0.88 (0.89) NS
Psychopharmacology (2009) 206:563–573 567

Table 2 Group means (SD) in

levels of superstitious Group Superstitious conditioning
conditioning on the
experimental phase across Block 1 Block 2 Block 3 All trials
individual blocks and all trials in
experiments 1 and 2 Experiment 1
Placebo Pre 5.50 (1.21) 5.38 (1.09) 4.88 (1.67) 11.19 (3.31)
Post 4.81 (1.11) 5.44 (1.03) 5.63 (1.41) 11.06 (3.40)
Low dose Pre 5.60 (1.18) 5.73 (1.71) 5.67 (1.40) 12.80 (4.70)
Post 5.27 (1.03) 5.67 (1.50) 5.53 (1.00) 12.00 (3.89)
High dose Pre 5.19 (1.33) 5.00 (1.67) 4.94 (1.34) 10.31 (3.65)
Post 5.88 (5.26) 5.25 (1.61) 5.50 (1.26) 12.06 (3.49)
Experiment 2
Ketamine users 5.56 (1.29) 6.72 (1.78) 6.00 (1.61) 18.28 (3.36)
Polydrug controls 5.37 (1.50) 5.47 (1.47) 4.89 (1.49) 15.74 (2.94)
Nondrug-using controls 3.94 (2.75) 5.82 (2.00) 5.06 (2.05) 11.53 (5.42)

bo, low dose, and high dose) and Order (version 1 first or Contrasts showed greater changes in the ketamine groups
version 2 first) as between subjects factors. No main effects compared to placebo (t45 =−4.49, p<0.001), and in the high-
were found for Block, Time, Group, or Order, and no dose compared to low-dose ketamine group (t45 =−4.28, p<
significant interactions emerged. 0.001). Negative symptoms: Analysis of negative symptoms
revealed a Group×Time interaction and main effects of
Questionnaire phase (Table 3) Due to low expected frequen- Group and Time. Subjects receiving placebo were at floor
cies, responses were collapsed into non-superstitious responses level at both pre-infusion and during the infusion. Contrasts
(“no” and “not sure”) and superstitious responses (“no, there again showed greater changes in the ketamine groups
were patterns but I didn’t find them” and “Yes”). Chi-squared compared to placebo (t45 =−2.53, p<0.05), and in the high-
tests showed no significant Group or Time effects. dose compared to the low-dose group (t45 =−2.51, p<0.05).
Anxious depression: There was a Group×Time interaction
and a main effect of Time. Contrasts between placebo and
Subjective effects (Table 4) ketamine groups revealed no significant ketamine effect.
Activation: No significant effects or interactions were found.
BPRS Neither ketamine nor norketamine plasma levels correlated
Positive symptoms: A 3×2-RMANOVA revealed a Group× with increased BPRS scores in the high-dose group.
Time interaction and main effects of Group and Time.
PSI
Table 3 Number of participants showing superstitious conditioning Perceptual distortions: A 3×2-RMANOVA revealed a
according to post-task responses for experiments 1 and 2 Group×Time interaction and a main effect of Time. Contrasts
Group Questionnaire response (n) revealed a significantly higher increase in scores during the
infusion in the ketamine groups than in placebo (t45 =−2.4,
Superstitious Non-superstitious p<0.05). Cognitive Disorganisation: There was a significant
Group×Time interaction and a main effect of Time. Contrasts
Experiment 1
showed a significantly higher increase in scores during the
Placebo Pre 13 3
infusion in both ketamine groups compared to the placebo
Post 13 3
group (t45 =−2.82, p<0.01). Delusory Thinking: There was a
Low dose Pre 11 4
main effect of time, indicating more distortion pre-infusion
Post 10 5
than during the infusion. No effects were found for
High dose Pre 12 4
Anhedonia or Mania, and scores on Paranoia were at a floor
Post 13 3
level. Neither ketamine nor norketamine plasma levels
Experiment 2
correlated with increased PSI scores in the ketamine groups.
Ketamine users 15 4
Polydrug controls 8 11 Correlations Within the two ketamine groups, Pearson
Non-drug using 4 13 correlations were conducted. In order to reduce the chance
controls
of type I error, these were conducted between degree of
568 Psychopharmacology (2009) 206:563–573

Table 4 Group means (SD) for subjective effects pre- and during the infusion

Subjective effect Group and time Group × Group Time

time
Placebo Low dose High dose

Pre During Pre During Pre During F (2,45) F (2,45) F (1,45)

BPRS
Positive 4.63 (0.72) 4.19 (0.54) 4.69 (0.87) 4.94 (0.77) 4.44 (0.63) 6.38 (1.36) 19.25*** 9.51*** 13.15***
symptoms
Negative 3.00 (0.00) 3.00 (0.00) 3.25 (0.58) 3.63 (1.03) 3.13 (0.34) 4.50 (1.86) 6.33** 5.21** 12.78***
symptoms
Anxious 7.69 (1.45) 6.44 (0.63) 8.31 (1.96) 6.81 (0.91) 7.06 (1.44) 7.75 (1.29) 8.43*** NS 8.34**
depression
Activation 3.13 (0.34) 3.25 (0.45) 3.06 (0.25) 3.06 (0.25) 3.31 (0.60) 3.31 (0.60) NS NS NS
PSI
Perceptual 1.00 (1.90) 1.31 (2.02) 0.56 (0.96) 2.44 (2.48) 1.25 (2.41) 3.94 (3.11) 3.25* NS 17.68***
distortions
Cognitive 6.50 (4.66) 5.50 (4.78) 4.13 (3.01) 6.25 (4.30) 5.13 (4.47) 9.44 (5.13) 4.78* NS 6.61*
disorganization
Delusory thinking 2.25 (2.44) 0.94 (1.34) 1.38 (2.00) 1.31 (2.24) 2.13 (2.19) 1.19 (1.68) NS NS 9.93**
Anhedonia 4.69 (2.52) 5.13 (2.71) 4.56 (3.01) 4.63 (2.47) 4.12 (2.16) 5.63 (3.91) NS NS NS
Mania 3.31 (1.54) 3.63 (1.63) 3.00 (1.32) 3.00 (1.71) 3.63 (2.94) 3.44 (1.71) NS NS NS
Paranoia 1.44 (1.46) 0.63 (1.31) 0.69 (1.01) 1.19 (2.29) 0.94 (0.77) 0.56 (0.73) NS NS NS

*p<0.05, **p<0.01, ***p<0.001

superstitious conditioning (range in frequency of pair choice)
across all blocks both pre-infusion and during the infusion and
the delusory thinking and paranoia subscales of the PSI. With
the alpha level Bonferroni-adjusted to 0.0125, only one
significant correlation emerged, and this was between pre-
infusion performance on the superstitious conditioning task
and paranoia during the infusion (r=−0.458, p=0.01). There
was also a trend for a correlation between level of
superstitious conditioning pre-infusion and delusory thinking
post-drug (r=−0.408, p=0.023).
Experiment 2: Chronic self-administered ketamine
Demographics (Table 5) Groups did not differ in age, gender,
or spot-the-word scores. A one-way ANOVA found group
differences in unusual experiences, cognitive disorganization,
impulsive nonconformity, and introvertive anhedonia.
Bonferroni-corrected contrasts showed that unusual experi-
ences was significantly higher among polydrug controls
compared to healthy controls (p<0.01), cognitive disorgani-
zation was higher among ketamine users compared to
healthy controls (p<0.001), and introvertive anhedonia was
higher among healthy controls compared to both ketamine
users (p<0.001) and polydrug controls (p<0.05).
Drug use (Table 6) Urinalysis results were consistent with
recently reported drug use. Healthy controls reported no
regular use of illicit drugs. The only significant difference
was that ketamine users reported using cannabis for more
years than polydrug controls (F1,36 =4.59, p<0.05).
All ketamine users reported regular use of ketamine,
administering a mean of 0.99 (±0.85) grams per session, for
3.30 (±2.92) years, 17.80 (±11.05) days per month, and last
used the drug 3.74 (±5.10) days before testing. Seven
polydrug controls reported to have tried ketamine between
28 days and a year prior to testing (mean 111.60 days, ±124),
but none had used it more than three times in their life. A
number of participants reported to have tried other drugs but
did not use them regularly.
Superstitious conditioning task Data were missing for one
participant from the ketamine group so data from the
superstitious conditioning task were analyzed with 18
ketamine users.
Experimental phase (Table 2) As in experiment 1, the
range in frequency of pair choice was used to index
superstitious conditioning in each of the three blocks of
the experimental phase. A 3×3-RMANOVA with Block
as a within subjects factor and Group as a between
subjects factor revealed a main effect of Group (F2,51 =
4.334, p<0.05) and a main effect of Block (F2,102 =5.706,
p<0.01) but no significant interaction. Planned compar-
isons showed that drug users (ketamine users and poly-
drug controls) showed greater levels of superstitious
Psychopharmacology (2009) 206:563–573 569

Table 5 Group means (SD) of participant demographic data in experiment 2

Ketamine users Polydrug controls Nondrug-using controls Group main effect

Age 21.00 (2.24) 20.95 (1.03) 21.23 (4.66) NS

Gender (N male/female) 16:3 10:9 10:7 NS
Spot the word 49.00 (3.11) 46.47 (9.20) 49.24 (4.52) NS
O-LIFE (total) 16.42 (4.19) 17.16 (6.53) 13.53 (5.94) NS
Unusual experiences 3.47 (1.95) 5.00 (3.09) 2.35 (2.59) F(2,52) =4.759*
Cognitive disorganization 6.84 (2.48) 5.00 (2.76) 3.12 (2.23) F(2,52) =9.864***
Impulsive nonconformity 4.32 (1.70) 4.58 (2.12) 3.82 (2.04) NS
Introvertive anhedonia 1.79 (1.87) 2.58 (1.92) 4.25 (1.95) F(2,52) =7.783***

*p<0.05, **p<0.01, ***p<0.001

conditioning—as indexed by a greater range in frequency Discussion

of pair choice—than healthy controls (p<0.01) and that
ketamine users showed higher levels of superstitious The main findings of this experiment were firstly that
conditioning than polydrug controls (p<0.05). Increased ketamine users and, to a lesser extent, polydrug controls
levels of superstitious conditioning among ketamine showed increased levels of superstitious conditioning
users compared to polydrug controls were still reliable compared to nondrug-using controls. This was evidenced
when years of cannabis use was entered as a covariate. both by their task responses in the objective learning phase
Years of cannabis use did not reach significance as a of the task and in their subjective responses about perceived
covariate, and no significant interactions emerged. Post patterns following the task. Secondly, although acutely
hoc analysis of Block with the alpha level adjusted to ketamine induced a range of psychotomimetic effects in
0.017 indicated that superstitious conditioning was healthy volunteers, it did not produce changes in supersti-
greater in block 2 than block 1 (p<0.01). A trend was tious conditioning compared with placebo.
also found for lower superstitious conditioning in block 3
compared to block 2 (p=0.064).
Table 6 Numbers of users and means (SD) for extent of drug use in
Questionnaire phase (Table 3) As in experiment 1, due to ketamine and polydrug control groups
low expected frequencies, answers were collapsed
Drug Ketamine users Polydrug controls
between non-superstitious responses (“no” and “not
sure”) and superstitious responses (“no, there were Cannabis
patterns but I didn’t find them” and “yes”). There were Number of users 19 19
significant group differences in the frequency of Last use (days) 125.00 (2.95) 77.10 (257.66)
superstitious and non-superstitious responses (χ2(2)= Amount per session (joints) 2.92 (3.04) 2.50 (1.80)
11.592, p< 0.01) with ketamine users reporting more Days used per month 14.53 (11.41) 17.39 (11.22)
patterns than polydrug controls (p<0.05) and polydrug Years used 4.45 (1.98) 2.81 (2.88)*
controls reporting more patterns than nondrug-using Ecstasy
controls (p<0.05). Number of users 19 17
Last use (days) 124.26 (250.70) 24.38 (23.92)
Correlations Within the ketamine group, Pearson corre- Amount per session (mg) 382.00 (252.65) 279.41 (196.10)
lations were conducted between degree of superstitious Days used per month 2.32 (2.26) 1.12 (1.53)
conditioning (range in frequency of pair choice) across Years used 2.70 (2.63) 1.28 (1.24)
all blocks, cognitive disorganization, introvertive anhe- Cocaine
donia, last use of ketamine, amount of ketamine used Number of users 16 17
per session, days per month of ketamine use, and days Last use (days) 117.94 (213.57) 159.00 (267.54)
since last use of ketamine. With the alpha level
Amount per session (mg) 387.50 (457.62) 217.68 (257.33)
Bonferroni adjusted to 0.00625 only one significant
Days used per month 0.25 (0.45) 0.77 (1.11)
correlation emerged and this was between cognitive
Years used 1.06 (3.34) 0.50 (0.97)
disorganization and days since last use of ketamine
(r=−0.646, p=0.003). *p<0.05
570
Acute ketamine and superstitious conditioning
Acutely, ketamine produced a number of psychotomimetic
effects compared to placebo, as evidenced by dose-
dependent increases in positive symptoms, negative symp-
toms and anxious depression on the BPRS, and increased
perceptual distortions and cognitive disorganization on the
PSI. These findings replicate similar observations following
acute ketamine on the BPRS (Krystal et al. 1994; Malhotra
et al. 1996; Newcomer et al. 1999).
No group differences were found for delusory thinking and
across the groups, scores on this subscale were higher pre-
infusion than during the infusion. In addition, paranoia was at
a floor level in all three groups, and no differences in
superstitious conditioning were observed, according to both
the stimuli chosen in the experimental phase and post-task
reports in the questionnaire phase. These results differ from
those of Corlett et al. (2006), who found that a low dose of
ketamine-disrupted prediction error signaling, visible as
changes in right lateral prefrontal cortical activation. Howev-
er, the behavioral data collected in the current study may have
not been sensitive enough to detect equivalent changes in
superstitious conditioning, and since Corlett and colleagues
did not index delusion-like beliefs at the initial low dose of
ketamine, it is difficult to compare these findings with ours.
Despite the absence of differences between the groups in
either symptoms or superstitious conditioning, we did find a
relationship between ketamine-evoked symptoms and base-
line levels of superstitious conditioning. Within the ketamine
groups in experiment 1, pre-infusion superstitious condition-
ing (range in frequency of pair choice) correlated negatively
with scores on the paranoia subscale of the PSI during the
infusion, and a trend was found for a negative correlation
between pre-infusion superstitious conditioning and post-drug
delusory thinking. Intriguingly, this may parallel findings of
Corlett et al. (2006), who showed that increased activation in
the rPFC to prediction error violation during placebo was
predictive of post-drug increases in related symptoms on the
PSE. One of the interpretations the authors proposed was that
individuals who are more sensitive to prediction errors may be
more vulnerable to the perturbation of this system by
ketamine. This explanation may hold true for experiment 1
in that individuals who are more sensitive to prediction errors,
evident here as lower superstitious conditioning pre drug, may
be more susceptible to perturbation of this system by
ketamine, observed in this study as greater ketamine-induced
paranoia and delusory thinking.
Chronic self-administered ketamine and superstitious
conditioning
The main findings of experiment 2 were that ketamine users
and, to a lesser extent, polydrug controls showed increased
Psychopharmacology (2009) 206:563–573
levels of superstitious conditioning compared to healthy
controls. Increased levels of superstitious conditioning
among ketamine users compared to polydrug controls, and
among all drug users compared to healthy controls, were
evidenced by a greater range in the frequency of pair
choices in the experimental phase and a greater number of
self reported “patterns” observed during the task. Experi-
ment 2 provides the first evidence that repeated use of
ketamine is associated with changes in superstitious
conditioning. Taken together with the incidence of delu-
sions in ketamine users observed in previous studies
(Morgan et al. 2009; Uhlhaas et al. 2007), these findings
may provide preliminary support for the theory that
superstitious conditioning underpins delusion-like belief
formation (King et al. 1984; Shaner 1999).
Participants did not differ in premorbid verbal IQ, age, or
gender, and the two drug-using groups were broadly
matched for other drug use other than ketamine. However,
the groups showed differences in trait schizotypy. Both
ketamine users and polydrug controls exhibited high levels
of positive schizotypy and low levels of negative schizo-
typy compared to nondrug-using controls, consistent with
previous findings among recreational drug users (Nunn et
al. 2001). Polydrug controls showed higher levels of
unusual experiences compared to ketamine users, which
was unexpected. Ketamine users scored more highly on
cognitive disorganization, an analog of thought disorder in
subclinical populations. This factor of the O-LIFE was
highly correlated with the recency of ketamine use, and
these findings concur with previous observations of thought
disorder among ketamine users (Curran and Morgan 2000;
Morgan et al. 2009).
The superstitious conditioning task and delusion formation
Pre-infusion levels of superstitious conditioning in experi-
ment 1 were related to subsequent ketamine-induced
symptoms; however, in experiment 2, psychotic-like symp-
toms in the ketamine group did not correlate with levels of
superstitious conditioning. This leaves some ambiguity as
to whether the superstitious conditioning task is indeed
tapping the early processes of delusion formation. To assess
delusions fully in ketamine users, future studies should
employ an additional measure such as the Peters Delusion
Inventory (Peters et al. 1999).
Ketamine users in experiment 2 reported using the drug
less (1.0 g/session for 3.3 years) than in Morgan et al. (2009),
in which frequent users reported to have used 3.8 g/session
for 6.1 years, and infrequent users reported to have used
1.3 g/session for 3.7 years. The observed group differences
in superstitious conditioning given relatively light ketamine
use in experiment 2 may be in line with the theory that
superstitious beliefs lie on a continuum with delusions
Psychopharmacology (2009) 206:563–573
(Brugger et al. 1994). However, future research comparing
heavy and light ketamine users or patient groups with
varying levels of delusional symptoms is needed to clarify
this matter. The superstitious conditioning task we
employed is language-independent, easy to administer, and
yields objective behavioral results. It could have a number
of practical applications if validated, for example, the
assessment of the early onset of delusions, a stage of the
disorder that is difficult to trace since the symptoms prior
to their formation are difficult to conceptualize (Jorgensen
1998).
Differences in performance observed on this task might
alternatively be understood in terms of the exploitation
versus exploration dilemma (for a review, see Cohen et al.
2007). During our task, participants had to choose whether
to exploit previous reward contingent choices by choosing
the same stimulus pairs repeatedly or to explore other pairs
that may or may not have a higher reward contingency.
Over the course of the task, a dominant pattern of
exploitation rather than exploration would be reflected by
stereotyped responding to certain stimuli and increased
levels of superstitious conditioning. Similarly, schizophren-
ic patients show “strategic stiffness” or the impaired
integration of choice outcomes over long periods of time
during decision-making tasks (Kim et al. 2007). In common
with other theories of delusion formation (Corlett et al.
2007; Kapur 2003), we believe that a failure to adapt to
changes in reward contingencies in one’s environment will
create a world of unpredictable circumstances, and delu-
sional beliefs are, thus, constructed in order to rationalize
these bizarre yet seemingly important events.
Superstitious conditioning among polydrug controls
Polydrug controls showed higher levels of superstitious
conditioning than healthy controls. This is not surprising
given that they reported regular use of other psychotomi-
metic drugs. Cannabis is considered an independent risk
factor in the development of psychosis (Moore et al. 2007),
and elevated schizotypy and delusions have previously
been reported by recreational cannabis users (Nunn et al.
2001). Meanwhile cocaine-induced psychosis (CIP) is well
established, and cocaine-dependent users can suffer from
transient delusions (Cubells et al. 2005). On the other hand,
chronic MDMA use is not thought to be associated with
increased levels of delusions (Montoya et al. 2002).
Acute and chronic ketamine as models of delusions
Acute ketamine has previously been shown to induce
delusion-like and referential beliefs among healty volun-
teers (Bowdle et al. 1998; Lahti et al. 2001; Pomarol-Clotet
et al. 2006; Corlett et al. 2006). However no changes in
571
superstitious conditioning or delusion-like symptoms were
observed following acute ketamine in the current study.
These apparent discrepancies may be due to different rating
scales used in different studies, which Pomarol-Clotet et al.
(2006) attempted to overcome using clinical interviews
based on the Present State Examination. However, clinical
interviews were beyond the scope of the current study.
Further, it should be noted that previous studies using
steady-state infusions have aimed for higher target plasma
ketamine levels of 200 ng/ml (Corlett et al. 2006; Pomarol-
Clotet et al. 2006) compared to 150 ng/ml in the current
study.
Based on the limited measures of psychopathology used
in this study, the findings from experiments 1 and 2 suggest
that chronic ketamine may provide a better model of one of
the processes theoretically involved in delusion formation
than acute ketamine. The findings of experiment 2 are
supportive of previous evidence of self-reported delusions
in recreational ketamine users and of both human and an
animal data suggesting that chronic exposure to NMDA
receptor antagonists is better able to model some aspects of
psychosis than acute exposure (Jentsch and Roth 1999;
Morgan and Curran 2006; Mouri et al. 2007). Furthermore,
it has been shown that repeated exposure to phencyclidine
can cause dysregulation of dopamine afferents to the
nucleus accumbens of rats (Jentsch et al. 1998), a
pathophysiology thought to underlie delusion formation in
superstitious conditioning theories (King et al. 1984;
Shaner 1999) and others (reviewed by Corlett et al. 2007).
Despite previous findings of delusion-like beliefs fol-
lowing acute ketamine and the clear advantages of acute
challenge studies over cross-sectional drug-user studies (for
example high control, within-subject manipulations, and the
use of healthy volunteers) a temporary pharmacological
manipulation may be limited in its contextual validity of
delusions in psychosis. Repeated exposure to ketamine, or
other psychotomimetic drugs, may provide a better model
of delusion formation since the nature of regular drug use
can precipitate a slow onset of psychotomimetic change, as
is the case in the emergence of psychosis. This possibility is
supported by recent findings that ketamine users showed a
profile of affective, perceptual, attentional, and cognitive
disturbances that was remarkably similar to that of
prodromal individuals who later transitioned to psychosis
(Morgan et al. submitted).
Limitations and future research
This study has a number of limitations. In experiment 1, a
high dropout rate meant that the planned target plasma
levels could not be used, and this might have reduced the
psychotomimetic effects of acute ketamine. Initially, we
aimed for 200 ng/ml plasma levels of ketamine in the high-
572
dose group and 100 ng/ml in the low-dose group. However,
due to a high dropout rate, these were reduced to 150 and
75 ng/ml, respectively. Nevertheless, increased BPRS and
PSI scores post-infusion reflect the successful induction of
psychotomimetic symptoms among both the low- and high-
dose groups compared to placebo.
Experiment 2 relied on naturalistic sampling of drug
users and, hence, may be confounded by other drug use,
problems in verifying drug use, and pre-existing differences
(Curran 2000). The observed group differences in trait
schizotypy are suggestive of pre-existing psychosis-
proneness, which might have accounted for group differ-
ences in superstitious conditioning. This possibility cannot
be ruled out since a longitudinal or prospective design was
not used. Because ketamine users were matched with
polydrug controls for other reported drug use, it is likely
that the heightened levels of superstitious conditioning seen
among ketamine users can be explained predominantly by
the chronic effects of ketamine. However, the interactive
effects of ketamine with other drugs cannot be ruled out.
Further research should assess superstitious conditioning in
cannabis- and cocaine-only groups in order to further
explore this issue.
The questionnaire phase of the superstitious conditioning
task may be limited in a number of ways. Firstly, since this
measure was included following completion of the task, it
reflects a retrospective overview of task responses over all
three blocks. In experiment 2, superstitious conditioning
increased between blocks 1 and 2 and appeared to decrease
by block 3. This suggests that perceived reward magnitude
changed during the course of the task. Including a
subjective measure of self-reported patterns following each
block of trials may have given a more accurate indicator of
superstitious beliefs during different stages of the task.
Another limitation is that participants did not rate their
confidence in their responses. Evaluation apprehension may
have led some participants to report patterns which they
were unsure of, and crucially, the experimental conditions
of experiments 1 and 2 may have accounted for differences
in these responses. Speculatively, the experimental con-
ditions of experiment 1, in which participants were assessed
under blind procedures in hospital and were connected to
various heart rate and blood pressure monitors as well as
the intravenous infusion, may have encouraged participants
to be more suggestible that they had seen patterns at this
stage of the task. In comparison, participants in experiment
2 were tested in the familiar environment of their own
homes and may have felt less pressure to respond in a
particular way.
It has been noted that negative reinforcement schedules
can lead people to believe they have more control over a
response-independent contingency (Aeschleman et al.
2003; Bloom et al. 2007) and both positive and negative
Psychopharmacology (2009) 206:563–573
reinforcers elicit striatal activation in response to prediction
error (Jensen et al. 2007). A superstitious conditioning task
might, therefore, be more sensitive to the formation of
delusional beliefs if it incorporated positive and negative
reinforcement schedules. Finally, differential financial
reward based on task responses has been incorporated into
salience attribution tasks used to index delusion-like beliefs
(Murray et al. 2008; Roiser et al. 2009). Future research
should, therefore, aim to determine whether superstitious
conditioning is more readily adopted when money—rather
than “points”— is utilized as a noncontingent reinforcer.
Summary of findings
In summary, the main findings of this study were that
repeated exposure to ketamine and, to a lesser extent,
polydrug use increased the propensity to adopt superstitious
conditioning, while acute ketamine did not induce changes
in delusory thinking or superstitious conditioning among
healthy volunteers. This study, therefore, replicated previ-
ous findings of delusions in ketamine users using a novel,
objective measure and subjective post-experimental reports.
Findings of increased superstitious conditioning among
polydrug users are in line with the psychotomimetic
profiles of cannabis and cocaine. If clinically validated,
our novel task assessing superstitious conditioning may
have important practical applications.
References
Aeschleman SR, Rosen CC, Williams MR (2003) The effect of non-
contingent negative and positive reinforcement operations on
the acquisition of superstitious behaviors. Behav Processes
61:37–45
Baddeley A, Emslie H, Nimmo-Smith I (1993) The spot the word test:
a robust estimate of verbal intelligence based on lexical decision.
Br J Clin Psychol 32:55–65
Bloom CM, Venard J, Harden M, Seetharaman S (2007) Non-
contingent positive and negative reinforcement schedules of
superstitious behaviors. Behav Processes 75:8–13
Bowdle TA, Radant AD, Cowley DS, Kharasch ED, Strassman RJ,
Roy-Byrne PP (1998) Psychedelic effects of ketamine in healthy
volunteers: relationship to steady-state plasma concentrations.
Anesthesiology 88:82–88
Brugger P, Dowdy MA, Graves RE (1994) From superstitious
behavior to delusional thinking: the role of the hippocampus in
misattributions of causality. Med Hypotheses 43:397–402
Clements JA, Nimmo WS (1981) Pharmacokinetics and analgesic
effect of ketamine in man. Br J Anaesth 53:27–30
Cohen JD, McClure SM, Yu AJ (2007) Should I stay or should I go?
How the human brain manages the trade-off between exploitation
and exploration. Phil Trans R Soc B 362:933–942
Corlett PR, Honey GD, Aitken MR, Dickinson A, Shanks DR,
Absalom AR, Lee M, Pomarol-Clotet E, Murray GK, McKenna
PJ, Robbins TW, Bullmore ET, Fletcher PC (2006) Frontal
responses during learning predict vulnerability to the psychoto-
Psychopharmacology (2009) 206:563–573
genic effects of ketamine: linking cognition, brain activity, and
psychosis. Arch Gen Psychiatry 63:611–621
Corlett PR, Honey GD, Fletcher PC (2007) From prediction error to
psychosis: ketamine as a pharmacological model of delusions. J
Psychopharmacol 21:238–252
Cubells JF, Feinn R, Pearson D, Burda J, Tang Y, Farrer LA, Gelernter
J, Kranzler HR (2005) Rating the severity and character of
transient cocaine-induced delusions and hallucinations with a
new instrument, the Scale for Assessment of Positive Symptoms
for Cocaine-Induced Psychosis (SAPS-CIP). Drug Alcohol
Depend 80:23–33
Curran HV (2000) Is MDMA (‘Ecstasy’) neurotoxic in humans? An
overview of evidence and of methodological problems in
research. Neuropsychobiology 42:34–41
Curran HV, Monaghan L (2001) In and out of the K-hole: a
comparison of the acute and residual effects of ketamine in
frequent and infrequent ketamine users. Addiction 96:749–760
Curran HV, Morgan CJA (2000) Cognitive, dissociative and psycho-
togenic effects of ketamine on recreational users on the night of
drug use and 3 days later. Addiction 95:575–590
Jensen J, Smith AJ, Willeit M, Crawley AP, Mikulis DJ, Vitcu I,
Kapur S (2007) Separate brain regions code for salience vs.
valence during reward prediction in humans. Hum Brain Mapp
28:294–302
Jentsch JD, Roth RH (1999) The neuropsychopharmacology of
phencyclidine: from NMDA receptor hypofunction to the
dopamine hypothesis of schizophrenia. Neuropsychopharmacol-
ogy 30:201–225
Jentsch JD, Taylor JR, Roth RH (1998) Subchronic phencyclidine
administration increases mesolimbic dopaminergic system
responsivity and augments stress- and psychostimulant-induced
hyperlocomotion. Neuropsychopharmacology 19:105–113
Jorgensen P (1998) Schizophrenic delusions: the detection of warning
signals. Schizophr Res 32:17–22
Kapur S (2003) Psychosis as a state of aberrant salience: a framework
linking biology, phenomenology, and pharmacology in schizo-
phrenia. Am J Psychiatry 160:13–23
Kim H, Lee D, Shin YM, Chey J (2007) Impaired strategic decision
making in schizophrenia. Brain Res 1180:90–100
King R, Barchas JD, Huberman BA (1984) Chaotic behavior in
dopamine neurodynamics. Proc Natl Acad Sci U S A 81:1244–
1247
Krystal JH, Karper LP, Seibyl JP, Freeman GK, Delaney R, Bremner
JD, Heninger GR, Bowers MB, Charney DS (1994) Subanes-
thetic effects of the non-competitive NMDA-antagonist, ket-
amine, in humans. Arch Gen Psychiatry 51:199–214
Lahti AC, Weiler MA, Tamara Michaelidis BA, Parwani A, Tamminga
CA (2001) Effects of ketamine in normal and schizophrenic
volunteers. Neuropsychopharmacology 25:455–467
Malhotra AK, Pinals DA, Weingartner H, Sirocco K, Missar CD,
Pickar D, Breier A (1996) NMDA receptor function and human
cognition: the effects of ketamine in healthy volunteers. Neuro-
psychopharmacology 14:301–307
Mason O, Linney Y, Claridge G (2005) Short scales for measuring
schizotypy. Schizophr Res 78:293–296
Mason O, Morgan CJA, Stefanovic A, Curran HV (2008) The
Psychotomimetic States Inventory: A new measure of psychotic-
type experiences. Schizophr Res Psychol Med 19:1–6
Matute H (1994) Learned helplessness and superstitious behavior as
opposite effects of uncontrollable reinforcement in humans.
Learn Motiv 25:216–232
Montoya AG, Sorrentino R, Lukas SE, Price BH (2002) Long-term
neuropsychiatric consequences of "ecstasy" (MDMA): a review.
Harv Rev Psychiatry 10:212–220
Moore TH, Zammit S, Lingford-Hughes A, Barnes TR, Jones PB,
Burke M, Lewis G (2007) Cannabis use and risk of
573
psychotic or affective mental health outcomes: a systematic
review. Lancet 370:319–328
Morgan CJ, Curran HV (2006) Acute and chronic effects of ketamine
upon human memory: a review. Psychopharmacology (Berl)
188:408–424
Morgan CJA, Monaghan L, Curran HV (2004) Beyond the K-
hole: a 3-year longitudinal investigation of the cognitive and
subjective effects of ketamine in recreational users who have
substantially reduced their use of the drug. Addiction
99:1450–1461
Morgan CJ, Muetzelfeldt L, Curran HV (2009) Ketamine use,
cognition and psychological wellbeing: a comparison of frequent,
infrequent and ex-users with polydrug and non-using controls.
Addiction 104:77–87
Mouri A, Noda Y, Enomoto T, Nabeshima T (2007) Phencyclidine
animal models of schizophrenia: approaches from abnormality of
glutamatergic neurotransmission and neurodevelopment. Neuro-
chem Int 51:173–184
Murray GK, Corlett PR, Clark L, Pessiglione M, Blackwell AD,
Honey G, Jones PB, Bullmore ET, Robbins TW, Fletcher PC
(2008) Substantia nigra/ventral tegmental reward prediction
error disruption in psychosis. Mol Psychiatry 13:239267–
239276
Nelson HE (1982) National Adult Reading Test (NART): test manual.
NFER, Nelson, Windsor
Newcomer JW, Farber NB, Jevtovic-Todorovic V, Selke G,
Melson AK, Hershey T, Craft S, Olney JW (1999)
Ketamine-Induced NMDA receptor hypofunction as a model
of memory impairment and psychosis. Neuropsychopharma-
cology 20:106–118
Nunn JA, Rizza F, Peters ER (2001) The incidence of schizotypy among
cannabis and alcohol users. J Nerv Ment Dis 189:741–748
Ono K (1987) Superstitious behavior in humans. J Exp Anal Behav
47:261–271
Overall JE, Gorham DR (1962) The brief psychiatric rating scale.
Psychol Rep 10:799–812
Peters ER, Joseph SA, Garety PA (1999) Measurement of delusional
ideation in the normal population: introducing the PDI (Peters et
al. Delusions Inventory). Schizophr Bull 25:553–576
Pomarol-Clotet E, Honey GD, Murray GK, Corlett PR, Absalom AR,
Lee M, McKenna PJ, Bullmore ET, Fletcher PC (2006)
Psychological effects of ketamine in healthy volunteers. Phe-
nomenological study. Br J Psychiatry 189:173–179
Roiser JP, Stephan KE, den Ouden HE, Barnes TR, Friston KJ, Joyce
EM (2009) Do patients with schizophrenia exhibit aberrant
salience? Psychol Med 39:199–209
Rudski J (2001) Competition, superstition and illusion of control. Curr
Psychol 20:68–84
Schafer SL, Vervel JR, Aziz N, Scott JC (1990) Pharmacokinetics of
fentanyl administered by computer controlled infusion pump.
Anaesthesiology 73:1091–1102
Shaner A (1999) Delusions, superstitious conditioning and chaotic
dopamine neurodynamics. Med Hypotheses 52:119–123
Skinner BF (1948) Superstition in the pigeon. J Exp Psychol
38:168–172
Solowij N, Hall W, Lee N (1992) Recreational MDMA use in Sydney:
a profile of "Ecstasy" users and their experience with the drug. Br
J Addict 87:1161–1172
Stefanovic A, Brandner B, Klassen E, Cregg R, Nagaratnam M,
Bromley L, Das RK, Rossell SL, Morgan C, Curran HV (2009)
Acute and chronic effects of ketamine on semantic priming:
modelling schizophrenia? J Clin Psychopharmacol 29(2):124–133
Uhlhaas PJ, Millard I, Muetzelfeldt L, Curran HV, Morgan CJ (2007)
Perceptual organization in ketamine users: preliminary evidence
of deficits on night of drug use but not 3 days later. J
Psychopharmacol 21:347–352