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Psychogenic explanations of physical illness: Time to examine the evidence

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Psychogenic explanations of physical illness: Time to examine the evidence

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Perspectives on Psychological Science 2016, Vol. 11(5) 606–631.
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Perspectives on Psychological Science
2016, Vol. 11(5) 606 –631
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DOI: 10.1177/1745691616645540
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In a significant proportion of patients with chronic physi-
cal complaints, detailed examination fails to reveal a well-
recognized disease process. In this situation, the physician
may suspect a psychological cause. Indeed, in neurologi-
cal clinics alone, an estimated 9%–11% of patients receive
a diagnosis suggesting a probable psychological cause
(Carson et al., 2000; Lempert, Dieterich, Huppert, &
Brandt, 1990), and an estimated 4%–22% of patients in
seizure clinics are diagnosed with “psychogenic” seizures
(Benbadis & Hauser, 2000). In this article, we examine
whether such psychological causal explanations have evi-
dential support, focusing on illnesses presenting as neu-
rological disorders. We ask: What sort of evidence would
be required to provide positive support for a psychogenic
explanation of these illnesses? We see no reason why a
lower standard of evidence should apply to a psychologi-
cal than to a medical explanation. Clearly, psychological
causation cannot be demonstrated by the mere absence
of a confirmed disease diagnosis (argument from igno-
rance). Medical practitioners simply cannot assume that
the current knowledge of disease and its markers is 100%
perfect or that all complaints not otherwise accounted for
must have a psychological origin. Furthermore, from a
scientific perspective, psychogenic theories of illness are
conceptually complex, requiring significant psychological
dysfunction and often also specific learning experiences.
These theories therefore demand particularly strong
empirical justification.
For this review, we define a psychogenic explanation
as one in which (a) the primary causal factors are formu-
lated at a psychological level (e.g., distress, fears, beliefs,
attributions, or expectations) and (b) addressing these
factors could lead to major improvement or even com-
plete recovery. We first consider several conceptual issues
that are relevant to interpreting evidence on this topic.
We then examine the features of two major types of neu-
rological disorders commonly explained in psychogenic
645540PPSXXX10.1177/1745691616645540Wilshire, WardPsychogenic Explanations of Illness
research-article2016
Corresponding Author:
Carolyn E. Wilshire, School of Psychology, Victoria University of
Wellington, P.O. Box 600, Wellington, New Zealand
E-mail: Carolyn.Wilshire@vuw.ac.nz
Psychogenic Explanations of Physical
Illness: Time to Examine the Evidence
Carolyn E. Wilshire and Tony Ward
Victoria University of Wellington
Abstract
In some patients with chronic physical complaints, detailed examination fails to reveal a well-recognized underlying
disease process. In this situation, the physician may suspect a psychological cause. In this review, we critically
evaluated the evidence for this causal claim, focusing on complaints presenting as neurological disorders. There were
four main conclusions. First, patients with these complaints frequently exhibit psychopathology but not consistently
more often than patients with a comparable “organic” diagnosis, so a causal role cannot be inferred. Second, these
patients report a high incidence of adverse life experiences, but again, there is insufficient evidence to indicate a causal
role for any particular type of experience. Third, although psychogenic illnesses are believed to be more responsive to
psychological interventions than comparable “organic” illnesses, there is currently no evidence to support this claim.
Finally, recent evidence suggests that biological and physical factors play a much greater causal role in these illnesses
than previously believed. We conclude that there is currently little evidential support for psychogenic theories of illness
in the neurological domain. In future research, researchers need to take a wider view concerning the etiology of these
illnesses.
Keywords
psychogenic, somatic, somatoform, functional neurological disorder, psychogenic movement disorders, psychogenic
nonepileptic seizures
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Psychogenic Explanations of Illness 607
terms, and outline some prominent psychogenic accounts
of these disorders. Finally, we evaluate the evidence sup-
porting these theories. Although the article is structured
as a narrative review, in key sections we apply a more
systematic search method to identify studies meeting
specific criteria.
Theoretical and Conceptual Issues
Psychogenic theories make the strong claim that psycho-
logical factors play a primary causal role in the develop-
ment or maintenance of illness. Establishing causation—in
the absence of experimental control—is challenging. It is
not sufficient merely to demonstrate an association
between an outcome and a hypothesized causal factor
(e.g., illness and depression). It is also necessary to rule
out a primary causal relationship in the opposite direc-
tion (i.e., that the illness caused the depression). There is
also the possibility that some third, possibly unknown
factor might be responsible for the association. In addi-
tion, one must distinguish between causation and modu-
lation. For example, high temperatures can exacerbate
the symptoms of multiple sclerosis (Guthrie & Nelson,
1995), but that does not mean it causes the illness. Simi-
larly, anxiety, stress, and tiredness may precipitate epilep-
tic seizures (Spector, Cull, & Goldstein, 2000), but we
would never conclude that these are causes of epilepsy.
One argument often claimed in support of psycho-
genic illness models is that psychological distress com-
monly manifests itself as physical complaints. For example,
the psychological phenomena that characterize anxiety
disorders are often accompanied by muscle tension and
gastrointestinal symptoms (Aldao, Mennin, Linardatos, &
Fresco, 2010). Similarly, the sad feelings and negative
thoughts that define depression are often accompanied
by insomnia and fatigue (Beck, 1961; Ward, 2006). Conse-
quently, severe psychological distress might very possibly
lead to more chronic, debilitating physical symptoms.
However, there are problems with this reasoning. First,
the causal relationship between these psychological and
somatic phenomena remains unclear. For example,
insomnia may actually increase a person’s risk of devel-
oping depression (Riemann & Voderholzer, 2003). A fur-
ther problem is that only a small proportion of severely
psychologically distressed people develop chronic, debil-
itating physical illnesses of the kind examined in this
article. Conversely, many individuals with such illnesses
do not exhibit any significant psychopathology. To
explain these inconsistencies, additional psychological
variables must be proposed.
Two such variables are conversion and somatization.
Conversion refers to a process whereby psychological ten-
sion or conflict is “converted” into physical signs and symp-
toms (see Brown, 2005, for a review). Somatization refers to
a marked tendency to experience or express psychological
distress as bodily symptoms or to misinterpret normal bodily
sensations as signs of illness (Barsky, 1992; Lipowski, 1988).
This tendency may be heightened in those with anxiety,
depression, or a strong introspective focus. It has been sug-
gested that somatization may contribute to the development
of chronic physical complaints (Brown, 2004). Another pos-
sible contributor is alexithymia: A person who cannot rec-
ognize the physiological sensations that normally
accompany certain emotions may misinterpret them as
signs of illness (Taylor, Bagby, & Parker, 1991).
However, these concepts are problematic. The status of
somatization (and indeed conversion) as a psychological
construct rests entirely on indirect inference from self-
reported physical complaints. There are no measurable
affective or cognitive components. The concept also is
highly underspecified: No constraints have been placed on
which specific physical complaints should—and should
not—be considered indicative. It is commonly assumed that
any physical complaint without a medical explanation must
reflect somatization. Given our current incomplete under-
standing of disease and its markers, this assumption is dif-
ficult to justify.
“Psychogenic” Movement Disorders
and Seizures: Presenting Features
Multiple physical complaints have been attributed to psy-
chogenic causes (e.g., chronic pain, gastrointestinal dis-
turbances, fatigue, and even sensory disturbances). In the
neurological domain, names for such disorders include
functional neurological (symptom) disorder, conversion
disorder, hysteria, somatoform disorder, and somatic
symptom disorder and more specific terms for particular
presentations. Here we consider in detail two presenta-
tions that have been extensively studied: psychogenic
movement disorders (PMDs) and psychogenic nonepilep-
tic seizures (PNESs). Both are associated with a set of
well-defined presenting features, and both can be readily
compared with “organic” diseases with similar features.
PMDs may themselves take many forms, including
limb weakness, hemiparesis, tremor, dystonia, jerks,
Parkinsonism, or even complete paralysis. The primary
criterion is that the presentation (including test results)
should be inconsistent with any well-established neuro-
logical movement disorder. In addition, other “positive”
diagnostic signs are usually sought; the most common
are listed in Table 1. These signs provide reassurance that
the diagnosis is not based solely on negative criteria.
However, it is unclear whether they significantly impact
on diagnostic outcome (see, e.g., Morgante et al., 2012).
PMDs can be chronic and intractable. Follow-up studies
published since 1985 have reported that anywhere from
20% to 62% of PMD patients were the same or worse at
least 6 months later (for a review, see Gelauff, Stone,
Edwards, & Carson, 2013).
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608
Table 1. Presenting Features Often Used to Distinguish Psychogenic Movement Disorders (PMDs) and Psychogenic Nonepileptic Seizures (PNESs) From Their
Organic Counterparts
Feature or sign
Effectiveness in distinguishing
psychogenic from organic complaints Example studies
PMDs
Collapsing or give-way weakness: Limb
collapses suddenly with light pressure
Feature highly specific to PMDs Observed in 45% of patients diagnosed with conversion disorder;
absent in a mixed group of neurological patients (Daum et al., 2015).
Hoover’s sign (in limb paresis): Bad
limb is weak when actively moved but
much stronger when used to counter-
balance another movement
Feature highly specific to PMDs Present in a third of patients diagnosed with “conversion disorder”;
absent in a mixed group of neurological patients (Daum et al.,
2015).
Dragging gait: When patient walks, the
leg is dragged behind the body
Feature highly specific to PMDs but has a
low baseline rate of occurrence
Observed in 5% of patients with conversion disorder; absent in a
mixed group of neurological patients (Daum et al., 2015).
Distractibility (esp. in tremor): Movement
improves if the patient distracted
Difference in incidence is relative, not
absolute
About twice as common in psychogenic than in organic tremor
(Kenney et al., 2007).
Suggestibility: Movement improves with
encouragement or placebo
Difference in incidence is relative, not
absolute
Psychogenic tremor more likely to respond to a placebo intervention
than organic tremor, but group difference not significant (Kenney
et al., 2007).
Entrainment (in tremor): Tremor will fall
into rhythm with a repetitive move-
ment of the good limb.
Cannot be used to distinguish PMDs from
organic movement disorders
Response to entrainment test did not differ significantly between
psychogenic and organic tremor patients (Kenney et al., 2007).
PNESs
Patient can recall some elements of the
episode afterward
Feature highly specific to PNESs In nearly two thirds of PNES patients, a command given during the
seizure was at least partially recalled afterward (cf. only 4% of those
with complex partial seizures; Bell, Park, Thompson, & Radtke,
1998; see also Devinsky et al., 1996).
Seizures rarely occur during sleep Feature highly specific to PNESs Only 0%–1% of PNESs occur during EEG-confirmed sleep, whereas
epileptic seizures are common during sleep (Bazil & Walczak, 1997;
Orbach, Ritaccio, & Devinsky, 2003).a
Seizures can be readily induced through
suggestion
Feature highly specific to PNESs Khan et al. (2009): In 46% of PNES patients, a seizure was provoked
under hypnosis by asking the patient to imagine a typical event (cf.
only 12.5% of unmedicated epileptic controls; see also J. J. Barry,
Atzman, & Morrell, 2000). J. D. Slater, Brown, Jacobs, and Ramsay
(1995): A saline injection presented as having an almost certain
chance of bringing on a seizure provoked seizures in 91% of PNES
patients, but 0% of epileptic controls (see also Walczak, Williams, &
Berten, 1994).
Eyes are often closed during seizure Difference in incidence in PNES vs.ES is
relative, not absolute
Eyes less likely to be open at PNES seizure onset than in ESs (Syed
et al., 2011).
Awareness or responsiveness during
seizure
Differences in incidence is relative, not
absolute
Awareness during episode significantly more common in PNESs than
in ESs, and PNESs more likely to be intensified or alleviated by
behavior of others (Syed et al., 2011). Responsiveness never normal
in PNESs, but in 48% of events, patient could respond to at least
one command (cf. only 18% of complex partial seizures; Bell et al.,
1998).
(continued)
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609
Feature or sign
Effectiveness in distinguishing
psychogenic from organic complaints Example studies
Incontinence is rare during seizure Difference in incidence is likely to be
relative, not absolute (findings inconsistent
across studies)
Reported rates of incontinence vary widely across studies; some show
group differences, and others do not (see, e.g., Cragar, Berry,
Fakhoury, Cibula, & Schmitt, 2002; Oliva et al., 2008).a
Self-injury is rare during seizure Difference in incidence likely to be relative,
not absolute (findings inconsistent across
studies)
Reported rates of self-injury vary widely across studies; some show
group differences, and others do not (see, e.g., Cragar et al., 2002;
Hovorka, Nežádal, Herman, Neˇmcová, & Bajacˇek, 2007; Oliva et al.,
2008).a
Seizures commonly exceed 2 min in
duration
Does not distinguish PNESs from ESs PNESs not significantly more likely to exceed 2 min than ESs (Syed
et al., 2011).
Emotive vocalizations or crying during
seizure
Does not distinguish PNESs from ESs Crying rare in both PNESs and ESs; no significant group differences
(Syed et al., 2011).
Bizarre movements (e.g. pelvic thrusting)
during seizure
Does not distinguish PNESs from ESs Pelvic thrusting rare in both PNESs and ESs; no significant group
differences (Syed et al., 2011).
Note: The concluding statements about the usefulness of these features are drawn from an informal review of relevant studies where an appropriate organic control group was used and
where the examiners were blinded to diagnosis (for subjective measures only). ES = epileptic seizure; EEG = electroencephalography.
aExaminer blinding was not required for studies addressing these features because they do not rely on subjective judgement.
Table 1. (Continued)
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610 Wilshire, Ward
PNES are primarily defined by the absence of accom-
panying epileptiform discharges on electroencephalogra-
phy (EEG) during the seizure (after alternative medical
diagnoses have been ruled out). PNESs vary widely in
their presentation: They may present as periods of unre-
sponsiveness alone or may be accompanied by tremor
or, in some cases, gross motor movements or even vocal-
izations (Hubsch et al., 2011; see also Gröppel, Kapitany,
& Baumgartner, 2000). However, the mere absence of an
EEG signature is not a definitive diagnosis in itself, as it is
also absent in some types of epileptic seizures (e.g., orbi-
tofrontal and mesial frontal lobe seizures; Saygi, Katz,
Marks, & Spencer, 1992). Consequently, certain positive
distinguishing signs are also sought, if possible, with con-
tinuous video EEG monitoring. The most common of
these are listed in Table 1. However, in practice, positive
features are generally used in a confirmatory way; their
absence is rarely sufficient to disconfirm a psychogenic
diagnosis.
PNESs can also be chronic and intractable. Studies
conducted after 1985 have reported that from 48% to 65%
of PNES patients continue to experience seizures 1 year
or more after diagnosis (considering studies of 30 patients
or more; see Bodde, Brooks, Baker, Boon, Hendriksen,
Mulder, & Aldenkamp, 2009).
Psychogenic Theories of Illness
Various theories have been put forward to explain the
symptoms observed in these disorders. Virtually all of
these meet our working definition of psychogenic—that
is, they propose that the primary causal (and/or main-
taining) factors are psychological. Classic psychodynamic
theories of these illnesses center on the concepts of dis-
sociation and conversion (see, e.g., Nijenhuis, 2001;
Prigatano, Stonnington, & Fisher, 2002; Sierra & Berrios,
1999; C. Spitzer, Spelsberg, Grabe, Mundt, & Freyberger,
1999). Here, the term dissociation refers to a process
whereby distressing memories or thoughts are excluded
from conscious awareness, enabling the person to avoid
distress. However, these cognitions continue to create
psychological tension at an unconscious level, which
may be relieved through physical signs and symptoms
(i.e., conversion). These can include movement abnor-
malities or, in cases of acute distress, even a seizure. Ill-
ness behavior may be further reinforced if the person
gains benefits such as sympathy, attention, or special
assistance (secondary gain).
More recent theories place less emphasis on trauma
and more on personality and learning. Brown (2004) pro-
posed that the central factor in psychogenic illnesses is a
tendency to experience certain normal bodily sensations
as unusually intense and to misinterpret them as signs of
illness. This is most likely to occur if the sensations have
personal salience—for example, the individual previ-
ously experienced them during a period of illness or dis-
tress or has thought about them or discussed them
extensively. However, these complaints are unlikely to
become severe and chronic unless the person also pos-
sesses certain psychological characteristics. These include
a tendency to focus attention on internal states (similar to
somatization) and a proneness to anxiety or depression
(which may heighten any introspective tendencies and
lead to rumination upon symptoms). According to Brown,
PMDs may occur if a person develops the false expecta-
tion that his or her movements will be limited or abnor-
mal in some way. This expectation may be incorporated
into an action plan, resulting in abnormal movements.
PNESs may occur when a single, aberrant action plan is
activated as an acute response to certain stimuli or expe-
riences. Having once been activated, the action plan then
is more readily reactivated under similar conditions in the
future.
Another, more recent account of PMDs also attributes
them to distorted expectations about one’s movement
capabilities (M. J. Edwards, Adams, Brown, Pareés, &
Friston, 2012). These expectations may be created in any
of the ways Brown (2004) suggested. However, the
expectations only lead to persistent movement difficul-
ties if there is great certainty attached to them—for exam-
ple, if a person is focused strongly upon internal bodily
functions or has developed intense health anxiety. In
these circumstances, the individual works unconsciously
to avoid disconfirmation of these expectations by adjust-
ing his or her movements to fulfill them.
Concerning PNESs, contemporary theories identify a
range of biological, psychological, and social factors that
may play a causal role in seizure development or mainte-
nance. These include past traumatic experiences, medical
history, psychological characteristics, and prior learning
(Bodde, Brooks, Baker, Boon, Hendriksen, & Aldenkamp,
2009; Bodde, Brooks, Baker, Boon, Hendriksen, Mulder,
& Aldenkamp, 2009; Reuber, 2009). However, again, the
individual’s psychological characteristics are crucial. Key
predisposing characteristics include a proneness to soma-
tization, a high level of anxiety or depression, difficulty
regulating emotion, or a maladaptive coping style. Per-
sons who have experienced epileptic seizures themselves
or observed them in others are particularly vulnerable
to PNESs, as they may “model” these previous experi-
ences when acutely distressed (symptom modeling; see
Aldenkamp & Mulder, 1997). Factors that further perpetu-
ate the occurrence of PNESs include negative affective
states, misattributions, avoidance of underlying psycho-
logical issues, and secondary gain (Reuber, 2009). These
various accounts recognize that different factors may
operate in different individuals. Indeed, Baslet (2011)
suggested two alternative sets of predisposing factors.
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Psychogenic Explanations of Illness 611
One is a proneness to somatization, combined with
extreme emotionality and suggestibility. The other is a
tendency toward dissociation, which when combined
with poor emotional awareness and limited cognitive
resources, may create a system more readily “tipped into
crisis.”
Testing Predictions of Psychogenic
Theories
In this review, we formulate a series of predictions based
on the theories previously described and examined the
existing evidence for each. We consider predictions relat-
ing to (a) psychological characteristics, (b) stressful or
traumatic life experiences, (c) illness features consistent
with a psychological origin (e.g., suggestibility), (d) sec-
ondary gain, and (e) the effectiveness of psychological
interventions. In the final sections, we consider some
other relevant sources of evidence, including whether
psychogenic diagnoses are stable over time and whether
there is evidence of accompanying biological abnormali-
ties in these individuals.
The role of psychological
characteristics
Virtually all theories we review predict a disproportion-
ately high incidence of anxiety, depression, and somati-
zation disorders in patients with PMDs and PNESs. Some
also predict high levels of introversion or a proneness to
dissociative experiences. Finally, several recent theories
predict marked disturbances in emotional regulation or
awareness, poor coping skills, or a high incidence of
associated personality disorders (e.g., borderline person-
ality disorder).
However, before such predictions can be tested, sev-
eral important methodological issues must be consid-
ered. One is that psychopathology can often be a
consequence, rather than a cause, of physical illness.
Indeed, even organic illnesses are associated with very
high rates of psychopathology (Katon, 2003). In one
large U.S. cohort study, researchers estimated that a major
(organic) disease diagnosis was associated with a 41%
higher likelihood of a recent diagnosis of depression or
anxiety (Cassem, 1995). Estimates are even higher for
conditions such as epilepsy (Gaitatzis, Trimble, & Sander,
2004) and Parkinson’s disease (Nuti et al., 2004). Further,
the risk of psychopathology increases in these diseases
with the number and severity of the physical complaints
(Kisely, Goldberg, & Simon, 1997; Kroenke et al., 1994).
Some portion of these associations may be a measure-
ment artifact. For example, the fifth edition of the Diag-
nostic and Statistical Manual of Mental Disorders (DSM-5;
American Psychiatric Association, 2013) criteria for depressive
disorders include disturbances of sleep, energy, concen-
tration, and appetite, all of which can be affected by
physical illness. Self-report scales also frequently contain
similar somatic items (e.g., the Beck Depression Inven-
tory–II: Beck, Steer, & Brown, 1996). Such schemes may
have a tendency to lead to overdiagnosis of psychiatric
problems in those with physical illnesses. Consequently,
to provide evidence concerning the causal role of psy-
chopathology in illness, investigators need to compare
the disorder of interest with one of known etiology with
similar physical complaints—and ideally, these com-
plaints should be of similar frequency and severity.
It also is important that the psychological or psychiat-
ric assessment is made independently of the medical
diagnosis. If the interviewer is aware the patient has
“medically unexplained” symptoms, his or her judgments
may be influenced in numerous subtle ways (e.g., a
patient worried about unexplained symptoms may be
rated as more anxious than one whose symptoms are
medically explained).
We systematically searched the literature for studies
that (a) included a control group with qualitatively simi-
lar symptoms due to organic disease and (b) had psycho-
logical measures that had been obtained independently
of the medical diagnosis, either by a blinded interviewer
or with an objectively scored self-report scale. We did not
require the control group to be fully matched on symp-
tom frequency and severity because to do so would have
yielded only one qualifying study in each illness domain,
but we did record this information. To ensure sufficient
power to detect differences, we further required at least
30 participants in the group of interest.1 Where there
were at least three studies with comparable measures
and samples, we also calculated average effect sizes (see
Supplementary Materials for full details of method).
Results. In the domain of movement disorders, there
were only the three qualifying studies (see Table 2). Rates
of self-reported depression and anxiety were higher, on
average, in PMD patients than in organic controls. Never-
theless, it is difficult to draw any firm conclusions from
such a small number of studies. Also, in two studies, con-
trols were patients with cervical or hand dystonia, which
may be painful and disabling but perhaps not fully com-
parable in psychological and functional impact to tremor,
myoclonus, or limb paresis.
In the domain of seizures, the outcomes of qualifying
studies are summarized in Table 3 (descriptions of each
study are presented in Tables S2–S4 in the supplementary
online materials). In the two studies in which an inter-
view format was used, one reported a reliably higher
incidence of anxiety and personality disorders (specifi-
cally, borderline personality disorder) in PNES patients
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612
Table 2. Studies Meeting Selection Criteria That Examined the Psychological Characteristics of Patients Diagnosed With Psychogenic Movement Disorders (PMDs)
Study name Patient groups
Construct
assessed Assessment methods Main findings
Control for
severity? Conclusion
Anderson
et al. (2007)
66 PMD (32 tremor, 10
dystonia, 10 myoclonus
and the remainder other);
704 OMD (Parkinson’s
disease)
Depression,
Anxiety,
Somatization
Depression, Anxiety,
and Somatization
scales from the Brief
Symptom Inventory
Higher mean scores in PMD than in
OMD group on all three scales.
Probably Depression:
yes
Anxiety: yes
Somatization:
yes
Kranick et al.
(2011)
64 PMD (tremors, gait/
balance disorders,
dystonia and weakness);
39 OMD (focal hand
dystonia)
Depression,
Anxiety,
Dissociative
experiences
Beck Depression
Inventory-II (BDI-II)
Beck Anxiety Inventory
(BAI)
Dissociative Experiences
Scale (DES)
Higher mean scores on BDI-II in
PMD than in OMD group.
Higher mean scores on BAI in
PMD group. Difference primarily
driven by neurophysiological items
(numbness, wobbliness, dizziness,
unsteadiness, trembling hands,
shakiness, and faintness).
No significant group differences on
DES.
Unclear Depression:
yes
Anxiety: yes
Dissociative
experiences:
no
Demartini
et al. (2014)
55 PMD (12 tremor, 12
myoclonus, 12 dystonia
16 weakness, 3 other);
33 OMD (majority cervical
or hand dystonia)
Depression,
Alexithymia
Montgomery-Asberg
Depression Rating
Scale (MDRS)
Toronto Alexithymia
Scale (TAS-20)
Higher mean scores in PMD than in
OMD group.
Higher mean scores in PMD than
in OMD group. 34% of PMD cases
qualified as alexithymic (scores
over 61), cf. 9.1% of OMD cases.
Unclear Depression:
yes
Alexithymia:
yes
Note: The Brief Symptom Inventory is from Derogatis (2000); Beck Depression Inventory–II (BDI–II) is from Beck, Steer, and Brown (1996); Beck Anxiety Inventory (BAI) is from Beck,
Epstein, Brown, and Steer (1988); Dissociative Experiences Scale (DES) is from Wiener (1992); Montgomery-Asberg Depression Rating Scale (MDRS) is from Montgomery and Asberg
(1979); Toronto Alexithymia Scale (TAS-20) is from Bagby, Parker, and Taylor (1994). PMD = movement disorder diagnosed as psychogenic; OMD = movement disorder with confirmed
organic basis.
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613
(continued)
Table 3. Summary of Findings From Studies Meeting Selection Criteria Examining the Psychological Characteristics of Patients Diagnosed With Psychogenic
Nonepileptic Seizures (PNESs)
Method used and
construct assessed
No. of
qualifying
studies
No. reporting
group differences
Groups equated
for seizure
frequency Instruments used Notes
Structured Clinical interview
Incidence of depressive
disorders
2 1 0 Structured Clinical interview based on DSM-III-R
or DSM-IV
Interviewers initially
blinded to medical
diagnosis, but this
information may have
been revealed during
the interview.
Incidence of anxiety and
anxiety-related disorders
2 0 0 As above
Incidence of borderline
personality disorder
2 1 0 As above
Self-report scale
Depression 14 6 0 BDI-II; Brief Symptom Inventory; MDRS;
Symptom Checklist; Cognitive Behavioural
Assessment (CBA); Hospital Anxiety and
Depression Scale (HADS); Profile of Mood
States (POMS); Minnesota Multiphasic Personality
Inventory–2 (MMPI-2) and/or Restructured Form
(MMPI-2-RF); NEO-Personality Inventory-Revised;
Personality Assessment Inventory (PAI); The
Depression Anxiety Stress Scale; Hamilton
Rating Scale for Depression (HRSD); Patient
Health Questionnaire.
Average effect size
was calculable from 4
studies using the PAI
Depression scale,
r = 0.161, p < .05
(see Table S5).
Anxiety 16 7 1 Symptom Check List; CBA Neuroticism and
State/Trait Anxiety scales; HADS; POMS;
MMPI-2 Psychaesthenia scale; Self-rating
Anxiety Scale; Spielberger State-Trait Anxiety
Inventory; Dimensional Assessment of Personality
Pathology Anxiousness scale; NEO-Personality
Inventory-Revised; Depression Anxiety Stress
Scale; MMPI-2-RF Negative emotionality/
neuroticism, Anxiety, and Stress/worry scales;
BAI; PAI Anxiety scale; Generalized Anxiety
Disorder scale.
An average effect size
was calculable from 4
studies using the PAI
Anxiety scale,
r = 0.134, p < .05
(see Table S5).
Introversion 3 0 0 MMPI-2 Social introversion scale; CBA introversion-
extraversion scale; NEO-PI-R extraversion scale.
Proneness to dissociative
experiences
6 3 0 Dissociative Experiences Scale (DES); The
Dissociation Questionnaire; Cambridge
Depersonalization Scale
Borderline personality
disorder
1 0 0 PAI Borderline scale
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614
Method used and
construct assessed
No. of
qualifying
studies
No. reporting
group differences
Groups equated
for seizure
frequency Instruments used Notes
Alexithymia or poor
emotional awareness
5 1 0 Toronto Alexithymia scale (TAS-20); Difficul-
ties in Emotion Regulation Scale (DERS) poor
emotional awareness and lack of emotional
clarity scales
Average effect size
calculable from 3
studies using the
TAS-20, r = 0.057, ns
(see Table S5).
Impulsivity 2 1 0 NEO-PI-R impulsiveness scale
Emotional lability or
dysregulation
2 1 0 Dimensional Assessment of Personality Patholo-
gy (DAPP-BQ); Affective lability scale; Difficul-
ties in Emotion Regulation Scale (DERS) poor
emotional regulation scale
Maladaptive coping skills
and/or defensive style
3 1 1 Response Evaluation Measure (REM-71); The
COPE: Assesses 15 typical coping styles; Multi-
dimensional Experiential Avoidance Question-
naire (measures defensive style)
Somatization or
conversion
11 11 1 PAI Somatic Complaints scale; Cognitive
Behavioural Assessment (CBA): Psychophysi-
ological Distress Scale; Somatization subscale
from Hopkins Symptom Checklist; Patient
Health Questionnaire ; Screening for Somato-
form disorders; MMPI-2 Hypochondriasis scale
and/or Somatic factor measure; Screening for
Somatoform Disorders-2; MMPI-2-RF Somatic
Complaints scale
Some studies reported
only a combined
measure for somatiza-
tion/conversion and
health anxiety. In
some studies, complaints
attributable to organic
disease were explicitly
excluded (see
Table S4)
“Dissociative” bodily
experiences
3 3 0 Somatoform Dissociation Questionnaire Average effect size
calculable from 3
studies using the DES,
r = 0.225, ns (see
Table S5)
Note: See Table S1 in the supplemental online materials for a detailed description of each study. The table also notes the number of studies where the PNES and control groups were
matched for seizure frequency. Full references to the scales and instruments used are presented in Table S2–S4 in the supplementary online materials.
Table 3. (Continued)
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Psychogenic Explanations of Illness 615
than in controls. No other reliable differences were
observed. Of course, despite initial blinding, the partici-
pants’ medical diagnosis was likely to have been revealed
during these interviews, so these assessments may not
have been entirely free of interviewer bias.
In the studies in which self-report measures were
used, results for anxiety and depression were inconsis-
tent. Some studies reported higher mean scores on self-
report measures of these constructs, but these studies
were outnumbered by those who reported null effects. In
studies in which average effect sizes were calculable, the
effects for both anxiety and depression were statistically
reliable but small (see Table S5 for details). It is interest-
ing to note that in studies where such data was available
and reported, the largest group differences on scales of
anxiety and depression were invariably observed on
physiological–somatic subscale items. In the three studies
in which introversion/extraversion was examined, no
reliable group differences were observed.
The findings with respect to dissociative disorders or
experiences were inconsistent, with half the studies
reporting group differences and the other half reporting
null effects. An average effect size, calculable from four
studies examining dissociative experiences, was not sta-
tistically significant (see Table S5).
With respect to emotional awareness and regulation, a
wide variety of constructs has been examined, but again,
findings were inconsistent across studies, with null find-
ings equaling or outnumbering reports of group differ-
ences. An average effect size was calculable from three
studies examining alexithymia; it was not statistically sig-
nificant (see Table S5).
Finally—in stark contrast to the findings discussed so
far—mean scores on scales measuring somatization and
related constructs were consistently higher for PNES
patients than for controls. One caveat is that it is not
always clear whether the evidence regarding somatiza-
tion was gathered independently from the medical diag-
nosis. In some studies, complaints attributable to organic
disease (e.g., epilepsy) were explicitly or implicitly
excluded, so the measure of interest is no longer inde-
pendent of the medical diagnosis.
It is worth noting that in those studies documenting
this information, PNES patients reported a considerably
higher frequency of seizures than epileptic controls (see
Tables S2–S4). This confound is of some concern: in epi-
lepsy, seizure frequency is a significant predictor of
depression and anxiety (see, e.g., Cramer, Blum, Reed, &
Fanning, 2003; Grabowska-Grzyb, Je˛drzejczak, Nagan´ska,
& Fiszer, 2006; Kimiskidis et al., 2007).
Discussion. If psychopathology played a primary
causal role in the development or maintenance of the
(severe) disorders considered here, we would expect
patients to score consistently and substantially higher on
the predicted psychological measures than organic con-
trols. Our review of the existing literature did not support
this prediction. With the exception of somatization
(which we discuss in more detail later), studies compar-
ing the psychological characteristics of PMD or PNES
patients with appropriate controls have not shown con-
sistent group differences. Where average effect sizes
were calculable, self-report measures of anxiety and
depression were slightly higher for PNES patients than
for controls, but the size of these effects was no greater
than we would expect on the basis of seizure frequency
alone.
The only psychological construct consistently associ-
ated with the illnesses of interest was somatization. Nev-
ertheless, this finding is difficult to interpret. The
measurement of somatization relies entirely on self-
reported physical complaints, which is problematic when
the groups being compared are not equated as to overall
disease severity or disability. Also, in some cases, physi-
cal complaints attributable to organic disease were
explicitly excluded, which rendered the group compari-
sons nonindependent. In addition, somatization itself is a
problematic construct because it assumes that all medi-
cally unexplained complaints must have a psychological
cause, which is a strong assumption given the incomplete
understanding of disease and its markers. Until there is a
way to define and operationalize somatization that is free
from these problems, this evidence must be interpreted
with extreme caution.
What is needed in the future to support claims about
the causal role of psychopathology in these illnesses is
(a) a theoretical framework that specifies exactly which
characteristics should and should not play a causal role;
(b) independent evidence concerning these characteris-
tics in the relevant population, preferably gathered prior
to illness onset; and (c) comparison against a control
group with symptoms of a similar nature, frequency, and
severity.
Stressful and traumatic life
experiences
Many theories propose that traumatic or stressful experi-
ences may predispose a person to psychogenic illness.
However, testing such predictions is far from straightfor-
ward. One problem is that even those with confirmed
organic disease report more adverse life events than
healthy individuals, and this tendency may simply reflect
a reporting bias (see Sharpe & Faye, 2006). Consequently,
any study that does not include a control group matched
for levels of physical disability is difficult to interpret.
One must also control for gender, since reporting rates
for physical and sexual abuse are generally higher in
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616 Wilshire, Ward
women (see Fiszman, Alves-Leon, Nunes, Isabella, &
Figueira, 2004). Age and socioeconomic status also need
to be considered, since both variables are likely to influ-
ence rates of abuse and other negative life experiences.
To identify studies in which at least some of these con-
cerns were addressed, we performed a systematic litera-
ture search applying the same quality criteria set out
previously but excluding studies in which the gender com-
position of the two groups differed widely (more than a
20-point difference in the percentage of females). We did
not set any criteria with respect to age and socioeconomic
status, but we have commented on this where relevant.
The qualifying studies are summarized in Table 4.
Only one study of PMDs met our quality criteria.
Kranick et al. (2011) examined 11 different childhood
and adult life experience variables. There were three sta-
tistically significant group differences likely to survive
correction for multiple comparisons: childhood emo-
tional (but not sexual) abuse, childhood physical neglect,
and overall incidence of lifetime traumatic events. How-
ever, it is unclear whether the control group used in this
study (those with focal hand dystonia) was sufficiently
well matched to the PMD group in terms of disability
severity.
Five studies of PNESs met our quality criteria. Two
interview-based studies showed a higher incidence of
sexual abuse in PNES patients than in epileptic controls.
One study focused on childhood events (Betts & Boden,
1992), and the other examined lifetime history (Scévola
et al., 2013). It is unclear whether the former study used
blinded interviewers; in the latter, interviewers were ini-
tially blinded to the medical diagnosis but may not have
remained so throughout the interview.
Three studies used written self-report measures. One
was difficult to interpret because the PNES patients were
considerably older than the controls, and age was found
to be an independent predictor of the key measures (van
Merode et al., 2004). In the remaining two studies, one
examined 13 life childhood and adult experience vari-
ables (Salmon, Al-Marzooqi, Baker, & Reilly, 2003). There
were three group differences likely to survive correction
for multiple comparisons: adult sexual abuse, childhood
psychological (not sexual) abuse, and control within the
family. However, once intercorrelations between these
variables were taken into account, the authors identified
only childhood psychological abuse as being uniquely
predictive of PNESs. In the final study, researchers exam-
ined recent stressful events in various domains (e.g.,
school, work, love, family, legal matters, and health) and
the distress they caused (Testa, Krauss, Lesser, & Brandt,
2012). No reliable group differences were found for any
of the key measures.
In conclusion, the existing evidence that adverse life
events play a causal role in suspected psychogenic
neurological illness is weak (see also Sharpe & Faye,
2006, for a similar conclusion). First, the number of well-
controlled studies in this domain is small. Second, inves-
tigators in these studies measured a wide range of
different variables and did not always agree on which
aspects of life history are most crucial (e.g., sexual vs.
psychological abuse). The problem here is theoretical as
well as empirical, since few psychogenic theories specify
which types of adverse experiences should and should
not be considered critical. Third, many of the variables
measured are strongly intercorrelated. For example, a child-
hood history of sexual abuse is strongly associated with
general family dysfunction, and both are strongly associ-
ated with low socioeconomic status (Rind, Tromovitch, &
Bauserman, 1998). Consequently, even consistent reliable
differences in personal history may be driven by factors
other than those being directly measured.
An even bigger problem is the reliance on retrospec-
tive self-report, which may be subject to recall or report-
ing bias. There is evidence that the recollection of past
experiences, especially negative ones, is strongly influ-
enced by one’s current state of mind (Merckelbach &
Muris, 2001). In addition, many patients with psycho-
genic diagnoses have been told their symptoms are due
to unresolved psychological problems, perhaps relating
to past experiences. Consequently, they are especially
likely to search for attributions from within their own life
history (see Briere, 1992; Pope & Hudson, 1995). What is
needed to demonstrate a causal role for adverse events is
(a) a model specifying the precise nature of the adverse
events that do—and do not—play a causal role in the
development of the illness and (b) prospective cohort
data, where measures relating to predefined adverse life
events can be obtained for the period before the onset of
illness (as well as demographic, medical, and psychiatric
information).
Presenting features suggestive of
psychological causation
Some of the positive presenting features associated with
PMDs and PNESs might themselves speak to illness etiol-
ogy. Table 1 summarizes the results of an informal review
of key studies of these features, where an appropriate
organic control group was included, and where examin-
ers were blinded to the medical diagnosis.
Two features were found to be highly specific to
PMDs, both of which pertain to cases of limb weakness:
Hoover’s sign and collapsing weakness. In Hoover’s sign,
the bad leg appears weak when the patient attempts to
move it but often is much stronger when it supports
other types of movements. In collapsing weakness, the
limb seems to give away suddenly upon light pressure.
Both features suggest psychogenic limb paresis may be
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617
Table 4. Studies Meeting Selection Criteria in Which Researchers Examined Aspects of Negative Life Experiences in Patients Diagnosed With a Psychogenic Movement
Disorder (PMDs) or Psychogenic Nonepileptic Seizures (PNESs)
Study subject/
researchers Patient groups Constructs assessed Assessment methods Main findings
Control for
frequency/
severity?
Interviewer
blinded to
medical diagnosis?
Movement disorders
Kranick et al.
(2011)
64 PMD
39 OMD, fully age- and
gender- matched to
PMD group)
(see Table 2 for details)
Childhood physical,
sexual, psychological
abuse; physical,
emotional neglect
Parental care and
overprotectiveness
Incidence of traumatic
episodes throughout
lifespan
Stress within the year
preceding illness
onset
Childhood Trauma
Questionnaire (CTQ)
Parental Bonding
Instrument (PBI)
Trauma Life Events
Questionnaire
Social Readjustment Scale
PMD group scored higher than OMD on:
physical and neglect, emotional abuse
(but not sexual abuse or emotional
neglect).
PMD group reported lower maternal care,
but higher paternal care; no other group
differences.
PMD group reported more adverse events
and episodes, and greater associated
fear.
No group differences.
Unclear na
Seizures
Betts and Boden,
(1992)
128 PNES (all female)
132 ES (all female)
Childhood sexual
abuse
Informal interview 54% of PNES patients reported at least
one corroborated sexual abuse event,
compared to 25% of ES controls.
No data on
seizure
frequency
Unknown
Scévola et al.
(2013)
35 PNES (77% female)
49 drug-resistant
epilepsy (59% female,
age matched)
Incidence of PTSD Structured Clinical
Interview I and II based
on DSM-IV
In 49% of PNES patients, lifetime trauma
history—specifically sexual abuse—met
DSM-IV criteria for PTSD, compared to
only 25% of ES controls.
No data on
seizure
frequency
Unclear if blinded
throughout
interview
Salmon,
Al-Marzooqi,
Baker, and Reilly
(2003)
81 PNES
81 ES, fully age and
gender matched
Physical, sexual,
psychological abuse
in both childhood
and adulthood
Parental care and
overprotectiveness
Family cohesion and
conflict
Medical history
questionnaire from Dross-
man et al. (1990)
Parental Bonding
Instrument (PBI)
Family Environment Scale
(FES)
PNES group reported significantly more
childhood psychological physical and
sexual abuse episodes than ES.
PNES group endorsed more items relating
to parental overprotection; no other
differences.
PNES group scored lower than ES on
emotional expression subscale, and
higher on control (no differences on
cohesion, conflict, and independence
subscales).
No data on
seizure
frequency
na
van Merode et al.
(2004)
40 PNES (65% female)
138 patients with ES or
non-epileptic seizures
with established organ-
ic basis (50% female)
Childhood trauma,
including:
emotional abuse,
physical abuse, sexual
abuse, emotional
neglect and physical
neglect.
Childhood Trauma
Questionnaire (CTQ)
Overall CTQ scores were higher for PNES
than ES group. However, PNES group
were older than controls, and age was
found to be a significant independent
predictor of scores.
No data on
seizure
frequency
na
(continued)
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618
Study subject/
researchers Patient groups Constructs assessed Assessment methods Main findings
Control for
frequency/
severity?
Interviewer
blinded to
medical diagnosis?
Testa, Krauss,
Lesser, and
Brandt (2012)
40 PNES, 20 ES Stressful life events,
ability to cope with
stress
Psychiatric Epidemiology
Research Interview (PERI)
Life Events Scale: probes
stressful events in last
12 months or previous 4
years (e.g., school, work,
love, family, legal mat-
ters, finances, and health)
and how much distress
they caused.
No significant differences between PNES
and ES groups, either on number of
events experienced or on the dis-
tress caused. However, PNES patients
reported more distress than ES patients
related to legal difficulties and health
specifically.
A higher
frequency
of seizures
in PNES
group
na
Note: The Childhood Trauma Questionnaire (CTQ) is from Bernstein et al. (1994); Trauma Life Events Questionnaire is from Kubany et al. (2000); Parental Bonding Instrument (PBI) is from
Parker, Tupling, and Brown (1979); Social Readjustment Scale is from Holmes and Rahe (1967); Structured Clinical Interview I and II based on DSM-IV is from First, Gibbon, Spitzer, Williams,
and Benjamin (1997; First, Spitzer, Gibbon, & Williams, 1996); Family Environment Scale (FES) is from Moos (1974); Psychiatric Epidemiology Research Interview (PERI) Life Events Scale is from
Dohrenwend, Krasnoff, Askenasy, and Dohrenwend (1978). ES = epileptic seizure.
Table 4. (Continued)
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Psychogenic Explanations of Illness 619
more amenable to intentional or attentional factors than
is the case for organic movement disorders. Nevertheless,
one must bear in mind that some organic disorders can
also be modulated by intentional or attentional factors, so
this is not definitive evidence of psychogenic causation
(e.g., motor neglect: Buxbaum et al., 2004; Parkinson’s
disease: Landers, Wulf, Wallmann, & Guadagnoli, 2005).
Other positive signs in PMDs offer little insight, either
because they are so rare that they do not speak to psy-
chogenic illness as a whole (e.g., dragging gait) or
because they also occur with reasonable frequency in
organic illness and therefore cannot be considered reli-
able indicators of psychogenic etiology (e.g., distractibil-
ity, suggestibility, and entrainment).
Turning to seizures, our review revealed two features
that are highly specific to PNESs. First, patients are often
able to recall elements of the episode afterward, which
suggests that their awareness may be less severely com-
promised than is usual during an epileptic event. This
feature certainly suggests the operation of a distinctly dif-
ferent neural mechanism in PNESs, but its relevance to
the issue of psychological causation is unclear. Second,
PNESs rarely occur during sleep, which suggests they
may be under a higher degree of voluntary control than
epileptic seizures. Again, this feature could be attribut-
able to a number of factors (e.g., physiological differ-
ences between sleep and wakefulness and their associated
brain states, the presence or absence of external stimuli,
and the triggering role of affect and cognition), so its
interpretation is less than straightforward.
A third feature highly specific to PNESs is that they
may be more readily induced through suggestion. In at
least four studies with an appropriate control group,
researchers found that PNESs are more likely to be
induced through the use of a nocebo, or through the
patient’s own mental efforts, than epileptic seizures.
However, in these studies, investigators did not control
for baseline seizure rate, which is often considerably
higher in PNESs (see Tables S2–S4). Of course, the more
frequently a person experiences seizures, the higher the
probability of exhibiting one under any conditions.
Again, although these findings suggest PNESs may be
qualitatively different, they do not offer strong support
for a psychogenic causal explanation, since psychologi-
cal factors such as anxiety and stress can also precipitate
epileptic seizures (Spector et al., 2000). There is a risk
here of confusing causation with moderation.
Other proposed differences between PNESs and epi-
leptic seizures are relative rather than absolute, so they
do not provide reliable evidence as to causation (e.g.,
eye closure during seizure, awareness during event, and
frequency of self-injury or incontinence) or are not statis-
tically reliable (e.g., length of seizure and incidence of
bizarre movements or emotive vocalizations during
seizure).
In conclusion, some presenting features of PMDs and
PNESs appear to be useful for distinguishing them from
organic disorders. PNESs, in particular, appear to be quali-
tatively different events from typical epileptic seizures.
Therefore, from a diagnostic point of view, it makes sense
to document such features. However, the features them-
selves do not make a strong case for a psychogenic expla-
nation. In many instances, the link between the relevant
feature and the suspected cause is not made clear or is
open to alternative interpretations. What is needed to
make stronger claims is a theory that specifies the precise
mechanism that gives rise to the feature in question.
Presence of secondary gain
A core concept in many psychogenic theories is that of
secondary gain—the ancillary benefits obtained by
assuming the sick role. The person’s symptoms may
allow him or her to gain sympathy, attention, or assis-
tance or to avoid unpleasant situations or stress. If sec-
ondary gain can be demonstrated, it may provide positive
support for a psychogenic explanation.
Secondary gain is not easy to measure. It is usually
measured by identifying changes associated with the sick
role that might be potentially reinforcing, such as sympa-
thy, attention, or avoidance of work (but, of course,
whether these changes are actually reinforcing for any par-
ticular individual cannot be known). However, the inci-
dence of secondary gains is likely to be related to the
person’s overall level of physical disability, so a carefully
chosen comparison group—one composed of individuals
well matched for the level of incapacity—is essential. Stud-
ies compared secondary gain in suspected psychogenic
illness with those in well-matched groups with neurologi-
cally confirmed disease have failed to show differences in
their incidence (Chabrol, Peresson, & Clanet, 1995; Gould,
Miller, Goldberg, & Benson, 1986). A further problem is
that secondary gains often are evaluated without taking
into account the associated losses, which may be wide and
devastating (e.g., loss of financial and personal indepen-
dence, loss of social contacts and leisure pursuits, and so
on). Clearly, gains must considerably outweigh losses if
they are to be motivating for the patient.
Finally, unless a set of objective criteria is applied inde-
pendently of the medical diagnosis, reporting can be sub-
ject to bias. To illustrate, a recent case report described a
young woman diagnosed with conversion disorder whose
physical symptoms were so debilitating that she required
residential care (Solvason, Harris, Zeifert, Flores, &
Hayward, 2002). In the original report, several secondary
gains were identified: the woman’s sickness role gave her
the chance to rebuild her relationship with her estranged
family and ex-lover and also provided relief from the
stress of working. The woman died shortly thereafter and
was found on autopsy to have Creutzfeldt–Jakob disease,
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620 Wilshire, Ward
a rare degenerative neurological disorder. This case illus-
trates how readily secondary gains can be found—even in
severe organic illness—and the dangers of seeking them
after a psychogenic diagnosis has been made.
Effect of psychological interventions
According to interventionist theories of causation
(Woodward, 2007), an illness in which psychological fac-
tors play a primary causal role should respond substan-
tially to an intervention targeting those factors, such as
psychotherapy. Several studies of PMD patients have
reported reductions in physical symptoms following vari-
ous forms of psychotherapy, including combined psy-
chodynamic psychotherapy and psychopharmacological
treatment (Hinson, Weinstein, Bernard, Leurgans, & Goetz,
2006) and hypnosis (Moene, Spinhoven, Hoogduin, & van
Dyck, 2002). In those with PNESs, reductions have been
reported following psychodynamic psychotherapy (Hinson
et al., 2006; Mayor, Howlett, Grünewald, & Reuber, 2010),
general psychotherapy (Brooks, Goodfellow, Bodde,
Aldenkamp, & Baker, 2007), and cognitive behavioral
therapy (CBT; Goldstein, Deale, O’Malley, Toone, &
Mellers, 2004; LaFrance et al., 2009).
However, few of these studies were randomized clini-
cal trials, so they might very possibly represent overesti-
mates of the effectiveness of these interventions (see
Staines & Cleland, 2007, for discussion). Also, very few
considered the possible impact of dropouts, which can
be very high in this domain (up to 30% or 40%; see, e.g.,
Chen et al., 2014; Kompoliti, Wilson, Stebbins, Bernard,
& Hinson, 2014) and are very likely to be nonrandom
(for discussion, see Jüni, Altman, & Egger, 2001; Montori
& Guyatt, 2001).
Therefore, to gain a more accurate picture of the effec-
tiveness of psychotherapy on the physical symptoms of
PNES and PMDs, we systematically searched the litera-
ture for studies that met the following criteria: (a) random
allocation of participants to a treatment or control condi-
tion (other than waitlist); (b) use of intention-to-treat
analysis, in which dropouts were counted as treatment
failures; and (c) at least 15 patients in the treatment arm
(although we also noted any qualifying studies with
lower sample sizes). One study met these criteria; its par-
ticipants were PNES patients. Goldstein et al. (2010) allo-
cated 66 PNES patients to either standard medical care
alone or accompanied by CBT. The CBT group showed a
reliably larger reduction in seizure frequency than the
control group at end of treatment (4 months) and at
6-month follow-up. One other study met all our criteria
except for sample size. In a pilot study, LaFrance et al.
(2014) used a two-way design to examine the effect of
CBT or treatment with sertraline on seizure frequency in
PNES patients. However, due to the small sample size (no
more than 10 patients per treatment arm), between-group
comparisons were not performed.
We conclude that evidence for the effectiveness of
psychotherapy in these disorders is weak. This conclu-
sion is in line with recent systematic reviews (PNESs:
Martlew, Pulman, & Marson, 2014; conversion disorder:
Ruddy & House, 2005).
The reader should also bear in mind that psychother-
apy, particularly CBT, has demonstrated broad effective-
ness in reducing physical symptoms even in organic
diseases, including epilepsy (for a review, see Tang,
Michaelis, & Kwan, 2014), and at least one such study
meets the minimum quality requirements we set out
(McLaughlin & McFarland, 2011). Few would assume that
such interventions modify the underlying causes of epi-
lepsy. More likely, they operate via a moderator variable.
Therefore, in order for researchers to distinguish causa-
tion from mere modulation of symptoms, a treatment
intervention would need to induce greater symptomatic
improvement in suspected psychogenic cases than in
organic controls. To our knowledge, no studies to date
have examined this question.
Stability of psychogenic diagnoses
over time
It has been suggested that some presentations diagnosed
as psychogenic may actually represent the early subclini-
cal manifestations of organic disease (E. T. Slater &
Glithero, 1965). Indeed, in studies conducted prior to
1970, researchers reported that between 10% and 30% of
neurological patients receiving a psychogenic diagnosis
were diagnosed later with an organic disease that could
have explained their earlier symptoms (see Stone et al.,
2005, and references therein). However, since then, these
rates have been steadily decreasing. For studies of psy-
chogenic neurological disorders in general, where the
diagnosis was made after 1985 and where a formal re-
examination was conducted at least 2 years later, the
reported rates of diagnostic change ranged from 5% to
12% (e.g., Crimlisk et al., 1998; Moene et al., 2000; see
Stone et al., 2005). Considering seizures specifically, one
study reported a 14% change rate (those where a sole
PNES diagnosis was changed to definite or probable epi-
lepsy; Lempert & Schmidt, 1990).
These rates are an improvement over those in earlier
reports. However, there is a limit to what can be inferred
from an unchanged diagnosis alone. An organic diagno-
sis generally requires a higher standard of supporting
evidence than a psychogenic one, and for a patient to
fulfill the requirements at follow-up, significant new evi-
dence is needed. A failure to find such evidence could
occur for many reasons, some of which have little to do
with the accuracy of the original diagnosis—for example,
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Psychogenic Explanations of Illness 621
the number and specificity of new presenting symptoms
or the ability of new diagnostic methods to reveal abnor-
malities that might have been missed previously. Conse-
quently, current rates of diagnostic change do not pose a
serious challenge to psychogenic theories, but neither do
they provide strong positive support for these theories.
Biological abnormalities and physical
precipitating events
Although psychogenic theories do not make specific pre-
dictions regarding the medical history of patients with a
psychogenic diagnosis, it is clearly worth considering this
issue. Table 5 summarizes the results of the key studies
reporting on these variables in PMDs and PNESs. Many
PMD patients have an accompanying organic movement
disorder (25% according to one study; Factor, Podskalny,
& Molho, 1995), and more than a third have a significant
neurological history. An even larger number report a phys-
ical injury or illness prior to PMD onset (up to 80% in
some studies).
Similarly, many PNES patients also suffer from epilep-
tic seizures. Exact estimates range from 5% to 30%,
depending upon whether the diagnosis required actual
observation of an epileptic seizure or merely a validated
history of epilepsy. Curiously, in one study of patients
with both epilepsy and PNES, frontal focal epileptic sei-
zures were unusually common, affecting around 25% of
such patients compared with only 4% of those with a
diagnosis of epilepsy alone (Pillai & Haut, 2012). PNES
patients also commonly exhibit abnormalities on struc-
tural magnetic resonance images. Finally, as with PMD,
the onset of PNESs is often preceded by an event such as
a head injury—or even surgery. It is interesting that such
events are also risk factors for epilepsy (Foy, Copeland, &
Shaw, 1981). In fact, in one study, investigators who ret-
rospectively examined individuals experiencing seizure-
like events after a head injury found that approximately
two thirds developed epileptic seizures, and the remain-
ing third developed PNESs (Hudak et al., 2004).
Many of these studies relied on retrospective self-
reports, which are subject to the recall biases outlined
earlier. Further, most did not include control groups, so it
is difficult to assess baseline rates of occurrence. There is
a need for further, more systematic investigation of these
variables. However, the evidence so far does suggest that
biological factors are likely to play a significant role in
the development of psychogenic neurological disorders.
Such findings have been accommodated within psy-
chogenic frameworks in various ways. It has been sug-
gested that illness or injury may itself be psychologically
traumatic, leading to feelings of helplessness, perhaps
triggering memories of earlier trauma (see Stone et al.,
2009, for discussion). Alternatively, previously
experienced illnesses may shape the manner in which
patients express current psychological distress (symptom
modeling: Bautista, Gonzales-Salazar, & Ochoa, 2008). A
third suggestion is that an earlier illness or injury might
increase a person’s general concern about bodily sensa-
tions (see, e.g., Brown, 2004), or the illness might shape
a person’s expectations about his or her present capabili-
ties (Pareés et al., 2013).
Other findings are difficult to explain within a psycho-
genic framework. One example is the development of
PNESs after surgery. Glosser, Roberts, and Glosser (1999)
suggested that the psychological distress patients experi-
ence at this time (a postsurgical period of “psychiatric
instability,” p. 1750) may be expressed by modeling pre-
vious epileptic episodes. In a similar vein, Pillai, Haut,
and Masur (2015) suggested that abnormalities involving
the orbitofrontal cortex may compromise emotional or
self-monitoring functions, which when combined with
trauma or other stressors, may increase a person’s sus-
ceptibility to psychogenic disorders. Both accounts
invoke different levels of explanation in service of a sin-
gle phenomenon: A neurological causal factor is used to
infer a psychological-level vulnerability, which in turn is
used to explain symptoms of an apparently neurological
nature. However, such evidence could quite reasonably
lead one to question whether simpler accounts might be
possible, in which psychological mediators play no role.
General Discussion
In this review, we sought to evaluate the evidence sup-
porting psychogenic theories of illness in the neurologi-
cal domain, applying the same evidence standards as one
would demand for any other causal explanation. Our
main conclusions were as follows. First, the incidence of
psychopathology is not consistently higher in these ill-
nesses than in comparable organic illnesses. The only
psychological characteristic found to be associated con-
sistently with a psychogenic diagnosis was somatization,
but there are major problems interpreting this association
(i.e., the nonindependence of the measures being exam-
ined and the untestable assumptions underlying the mea-
surement of somatization). Second, researchers in a small
number of studies have found that patients with a psy-
chogenic diagnosis report more adverse life experiences
than organic controls, but they disagree as to which types
of experiences are implicated. Also, reporting biases may
operate to exaggerate any group effects, and there are
problems teasing apart intercorrelated variables. Third,
although some of the presenting features of these ill-
nesses differ from those of comparable organic cases,
these differences are usually relative rather than absolute,
which limits their value as support for a psychogenic
explanation. Fourth, researchers examining whether
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622 Wilshire, Ward
Table 5. Summary of Results of Several Key Studies of the Precipitating Role of Illness or Injury in Psychogenic Movement
Disorders (PMDs) or Psychogenic Nonepileptic Seizures (PNESs) and the Incidence of Concomitant Organic Abnormalities
Study subject/researchers Main finding See also
Movement disorders
Factor, Podskalny, and
Molho (1995)
In a sample of 28 patients diagnosed with PMDs, 25% also had a
confirmed neurological movement disorder, often of the same
nature as the psychogenic one but involving a different body part.
Pareés et al. (2013);
Ranawaya, Riley, and Lang
(1990)
Crimlisk et al. (1998) In 73 such patients diagnosed with PMDs, 42% had a significant
neurological history. The most common events were disc surgery,
migraine, and peripheral nerve palsy.
Stone et al. (2009) This systematic review of previous studies found in 37% of patients
with PMD, a physical injury in some form was reported prior to
symptom onset, either by the patients themselves or in their
medical records.
van Hilten, Geraedts, and
Marinus (2007)
Pareés et al. (2014) In a sample of 50 patients with various PMDs, 80% reported an
illness or injury prior to the onset of the disorder, most commonly
a physical injury, an infection, or a neurological disorder.
Seizures
Reuber, Fernández,
Bauer, Singh, and
Elger (2002)
In a large sample of PNES patients (without concomitant ES),
8% showed interictal epileptiform discharges and a further 50%
showed other nonspecific EEG abnormalities. Further, in 27% of
the patients for whom MRIs were available, at least one of the
following abnormalities was observed: evidence of a surgical le-
sion, generalized atrophy, or evidence consistent with a previous
traumatic brain injury.
Reuber, Fernandez,
Helmstaedter, Qurishi,
and Elger (2002)
E. Barry et al. (1998) In a sample of 57 PNES patients, 24% had a documented head
injury within the three years preceding seizure onset.
See also Westbrook,
Devinsky, and Geocadin
(1998) for a similar estimate
Elliott and Charyton
(2014)
In a study of more than 300 PNES patients (none with concomitant
ES), 37% were found to have a history of head injury according to
their medical notes (Elliott & Charyton, 2014).
Glosser, Roberts, and
Glosser (1999)
In a sample of 250 patients who had undergone temporal lobectomy,
9% developed new psychogenic seizures following surgery.
Reuber, Kral, Kurthen,
and Elger (2002)
A retrospective study of 372 PNES patients showed that in 4.6% of
cases, PNES first started after intracranial neurosurgery.
Note: ES = epileptic seizure; EEG = electroencephalography; MRIs = magnetic resonance images.
PNESs are more inducible than epileptic seizures may fail
to control for differences in baseline seizure rate. They
also run the risk of confusing modulation and causation.
Finally, it is not yet known whether suspected psycho-
genic illnesses are more responsive to psychological
interventions than comparable organic illnesses.
Therefore, the overall conclusion from this review is
that there is insufficient evidence to support the view that
psychological factors are the primary causal or maintain-
ing factors in these disorders. Further, if we take into
account the effects of publication bias, which would
likely operate to exaggerate any apparent support for
psychogenic accounts, the “reality” may be even less
favorable to these accounts than this review indicate.
This is not to say that psychogenic explanations of these
illnesses cannot possibly be true but simply that the evi-
dence is current lacking. Perhaps the psychological line
of inquiry might eventually bear fruit if one searches long
and hard enough. However, the time may have come to
focus on lines of inquiry that could be more beneficial to
patients.
Our conclusion is not entirely at odds with historical
precedent. In medicine, there is an ever-lengthening list
of physical illnesses formerly attributed to psychological
causes that are no longer believed to be primarily psy-
chogenic. These include gastric ulcers (see e.g., Alp &
Grant, 1970), multiple sclerosis (Caplan & Nadelson,
1980; Langworthy, 1948), ulcerative colitis (McKegney,
Gordon, & Levine, 1970), rheumatoid arthritis (Moos,
1964); systemic lupus erythematosus (McClary, Meyer, &
Weitzman, 1955), and, most recently, postconcussive syn-
drome (King, 2003 vs. Gosselin et al., 2011; Shenton
et al., 2012). As new methodologies and diagnostic tech-
niques are developed, other illnesses are likely to be
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Psychogenic Explanations of Illness 623
added to the list. Nevertheless, our conclusion is clearly
at odds with the prevailing view in literature within this
domain, where one commonly sees strong statements
such as “Psychogenic nonepileptic seizures (PNES) . . .
have a psychological origin” (Brown et al., 2011, p. 85)
and “Psychogenic movement disorders (PMDs) are move-
ment disorders that result from a psychological or psychi-
atric rather than neurological disturbance” (Gupta &
Laing, 2009: p. 430).
There are a number of possible reasons for our differ-
ent conclusions. First, previous research has been
founded on the premise that these illnesses are indeed
psychogenic in origin. Researchers have not sought to
scrutinize that premise. In contrast, we made no prior
assumptions but instead carefully examined the support-
ing evidence from a fresh perspective. Second, in key
topic areas, we identified studies using a more systematic
method than is adopted in narrative reviews. Our method
may have provided some protection against citation bias,
the tendency for studies confirming a prevailing view-
point to be cited more often than those disconfirming it
(Greenberg, 2009; Jannot, Agoritsas, Gayet-Ageron, &
Perneger, 2013). Citation bias can become amplified over
time and through the mediating effect of influential nar-
rative reviews, creating a distorted picture of the evi-
dence (see, especially, Greenberg, 2009).
Third, we adopted a conservative approach to the
evaluation of the evidence. In each topic area, we first
identified potential problems in study design that might
compromise the conclusions. We then located those
studies that best addressed these problems. Finally, we
critically examined any remaining difficulties that might
impact on interpretation.
Some might object that our conservative approach has
“thrown the baby out with the bathwater.” Perhaps many
studies reporting genuine evidence were rejected as
flawed. Perhaps behavioral researchers need to adopt
more relaxed standards than other fields, since behavior
is so complex, noisy, and difficult to measure. Perhaps a
psychological explanation is harmless and offers some
comfort to the patient, irrespective of its accuracy. Our
response to these arguments is twofold. First, the sheer
noisiness of behavioral data should not be a justification
for applying lower standards of evidence but rather a
reason to adopt even greater care. Recently, there has
been growing concern within psychology that many of
its key findings may not be secure (see, Ferguson &
Heene, 2012; Ioannidis, 2012; Simmons, Nelson, &
Simonsohn, 2011). This has led to a call for generally
tighter standards of evidence.
Second, psychogenic explanations are far from harm-
less. At a population level, if practitioners falsely con-
clude that an illness is due to psychological factors,
research avenues may be pursued that are ultimately
unfruitful, most likely at the expense of more valuable
ones—at a real cost in terms of future patients’ treatment
opportunities (see Davey-Smith, 2005, for discussion).
The patients’ own self-reports about their symptoms and
their precipitators, which may be a valuable source of
information about their illness, may be disregarded,
thereby further delaying progress.
There may also be serious risks for the individual
patient. From the moment a psychogenic explanation is
offered, the patient’s own perceptions about his or her
symptoms are recast as dysfunctional and become targets
for “correction” by those claiming greater insight. A psy-
chogenic interpretation also carries implications about
the patient’s own responsibility for the continuing illness.
Behavioral therapies may reinforce that message, and a
failure to respond to therapy may sometimes even be
blamed on the patient (“The patient’s own psychopathol-
ogy interferes with treatment”: Harden, Burgut, & Kanner,
2003, p. 454). If these illnesses turn out not to be of psy-
chological origin, such approaches are clearly inappro-
priate and potentially highly damaging to the individual.
Indeed, frequent themes in the narratives of those diag-
nosed with a psychogenic illness are (a) a feeling that
their own reports of their symptoms have not been suf-
ficiently heard and considered (e.g., Barnum, 2014;
Karterud, Knizek, & Nakken, 2010), (b) distress or anger
at the suggestion they are psychologically unstable
(Fairclough, Fox, Mercer, Reuber, & Brown, 2014; Karterud
et al., 2010), and (c) feelings of self-blame for being
unable to control their illness (Nettleton et al., 2005).
These themes do not appear to reflect any specific psycho-
pathology related to psychogenic illness, since they also
appear in the narratives of patients who later received an
organic diagnosis (e.g., multiple sclerosis: R. G. Edwards,
Barlow, & Turner, 2008; Ehler–Danlos syndrome: Barnum,
2014; and Sneddon’s syndrome: Mildon, 2015).
A psychogenic diagnosis also influences the way
patients are viewed by others. Findings in studies in which
artificial patient vignettes were used suggest that a patient’s
complaints may be rated as less serious if they are believed
to be psychogenic, and the patient is more likely to be
characterized negatively (De Ruddere et al., 2014; De
Ruddere, Goubert, Stevens, Williams, & Crombez, 2013).
Most important, psychogenic explanations also have
serious practical consequences. Many experts advocate
the minimization of disability aids in such cases, since
they may reinforce false illness beliefs or provide second-
ary gains (Davison, Sharpe, Wade, & Bass, 1999). Such
denial of support would be a catastrophic error if the
person’s disability were in fact intractable. A psychogenic
explanation also may affect the patient’s future medical
care. It is often recommended that further medical inves-
tigations be minimized (Deary, Chalder, & Sharpe, 2007;
Hotopf, 2004). Physicians also may be more inclined to
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624 Wilshire, Ward
attribute any future physical complaints to psychological
causes. Both these factors could combine to delay diag-
nosis and treatment of underlying or subsequently devel-
oping disease. Although there are no systematic studies
of this issue, one recent survey of 12,000 patients with
rare diseases showed that a psychological or psychiatric
misdiagnosis substantially increased time to correct diag-
nosis compared with a nonpsychological misdiagnosis—
in some illnesses, by more than 5 years (Kole & Faurisson,
2009).2
Given the insufficient supporting evidence and the
dangers of making an incorrect inference, we recom-
mend researchers and practitioners refrain from claiming
that the illnesses we have considered here have a psy-
chological cause. Until better evidence exists, their
causes are simply unknown. Also, the terms used to
describe these illnesses (e.g., psychogenic) convey a
sense of certainty about the underlying cause, which is
extremely misleading in the light of current evidence.
We recommend the alternative terms nonepileptic attack
disorder, functional movement disorder, or functional
neurological disorder, which although not entirely free
of connotations, at least do not make explicit reference
to psychological factors.
In this review, we identified a number of problems
with current research approaches in this domain. These
include the problems in teasing apart the direction of
causal relationships within observational studies; the dif-
ficulties associated with inferring psychological traits
from physical complaints alone (e.g., somatization); the
biases that can occur when the psychological and medi-
cal assessments are not performed independently; the
intercorrelated nature of many of the variables proposed
to play a causal role in these illnesses; and the problems
associated with retrospective self-report measures. To
obtain more reliable evidence about the role of psycho-
logical variables in illness, researchers may need to use
an entirely different approach. For example, by selecting
participants who possess the psychological characteris-
tics of interest before they exhibit any physical symp-
toms, investigators may be able to establish which of
these variables reliably predicts illness outcomes (both
explained and unexplained) at a later point.
Another serious problem concerns the “default” nature
of psychogenic explanations. There is a massive gap in
evidence standards required for classification of an ill-
ness as medically explained (organic) on the one hand
and as psychogenic on the other. The former requires
positive substantiating evidence and the latter little more
than the absence of evidence (we have seen that even if
positive signs are sought, these are unlikely to impact
substantially on diagnostic outcome). In practice, disor-
ders that fail to meet the criteria for a known organic ill-
ness readily slip through this evidence gap and become
presumed to be psychogenic by default. This category
becomes a wastebasket for any illness awaiting a full
explanation and is likely to be highly heterogeneous. It is
quite possible that some patients may suffer from a genu-
ine psychological problem, whereas others might have
some disease that is currently poorly understood; some
might even be feigning illness. The only way to address
these problems in future is to confront the unwarranted
assumption that all “unexplained” illnesses have a single
common cause. The next step is to seek positive criteria
that may help identify specific subgroups.
Finally, we also identified some significant problems
with existing theory in this area. Current psychogenic
theories are often phrased in such general terms that they
are difficult to falsify. For example, evidence suggestive
of a role for biological factors in this disease would seem
to call for a re-evaluation of certain theories. Instead, it
has been accommodated within existing theories without
alteration of their central tenets— for example, by pro-
posing that patients may “model” the symptoms of previ-
ous illnesses or that neurological abnormalities in turn
create “psychological vulnerabilities,” which in turn cause
the illness. The possibility of a simpler, more direct causal
relation is not considered. It is time to widen the net and
consider other possible explanations for these illnesses.
In the domain of PMDs, some new ideas are already
beginning to emerge. For example, it has recently been
suggested that pain may play a critical mediating role in
the development of some PMDs (Stone et al., 2009; van
Hilten, Geraedts, & Marinus, 2007). The central idea is
that the difficulty in movement develops gradually as a
direct response to complex and chronic pain. The mech-
anisms responsible operate at a subcortical level, engen-
dering a gradual change to movement behavior that is
outside the person’s awareness.
Another recent proposal is that some PMDs may arise
from inadequate top-down, goal-driven control of move-
ment (Voon, Brezing, Gallea, & Hallett, 2011). Conse-
quently, movement behavior is more easily shaped by
factors outside the person’s current goals and intentions
(including states of high emotional arousal). States of
high emotional arousal in particular may activate prob-
lematic, abnormal movement plans, which then may
compete for selection with the target movement. The
poor top-down control itself need not have a psychologi-
cal origin. It could be due to a loss of functionality within
brain networks responsible for movement—perhaps as a
consequence of an illness or injury—that may be difficult
to detect with standard diagnostic techniques (see Felicio
et al., 2010; Lang, Koller, & Fahn, 1995; Vuilleumier et al.,
2001, for studies that support this hypothesis).
In the domain of PNESs, there has been relatively little
consideration of the proximal neural mechanisms respon-
sible for the PNESs themselves. However, a better
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Psychogenic Explanations of Illness 625
understanding of these mechanisms is likely to reduce the
explanatory burden placed on psychological factors.
Research is beginning to make inroads here. In a recent
study by Arzy et al. (2014), EEG was used to record elec-
trophysiological activity during the actual PNESs of three
individuals. All had a dual diagnosis of PNES and epi-
lepsy. In all three, PNESs (but not epileptic seizures) were
associated with decreased theta band activity focused in
the left posterior parietal cortex. Given that theta band
activity of this kind is thought to indicate tight synchroni-
zation between frontal and parietal regions, such as is
required during cognitively demanding tasks (Sauseng,
Klimesch, Schabus, & Doppelmayr, 2005), its sudden
absence may be associated with a dramatic loss of cogni-
tive capability and perhaps even loss of awareness. In one
patient examined with implanted electrodes, the focus of
this theta change and the focus of his epileptic seizures
were in neighboring regions—a finding that calls into
question whether the two types of seizures really are
caused by entirely different mechanisms.
Of course, a key feature of both PMDs and PNESs is
likely to be heterogeneity, so researchers are probably
seeking not one explanation but several. In the case of
PNESs, some events may turn out to have a physiological
basis (e.g. cardiovascular events: Parra, Iriarte, & Kanner,
1999; Vossler, 1995; Zaidi, Clough, Cooper, Scheepers, &
Fitzpatrick, 2000), others may represent other types of
neurological events, and yet others may turn out to be
well-characterized psychophysiological events such as
panic attacks. Similarly, some PMDs may arise as a con-
sequence of peripheral factors, such as localized pain,
whereas others may be indicative of a more central neu-
rological disturbance. The disordered movements may
have been reinforced further through learning via sub-
cortical mechanisms. Again, acknowledging the hetero-
geneous basis of these disorders is likely to be crucial to
further progress.
Limitations
One major limitation of this study is that our conclusions
were based almost entirely on evidence from two disor-
ders: movement disorders and seizures. Many other com-
plaints have also been attributed to psychological causes,
from chronic pain and fatigue to visual and somatosen-
sory disturbances. Most of the interpretational issues
identified here apply equally to these other conditions
but not necessarily its more substantive conclusions. The
next step in this research is to extend the approach to
other illnesses that are commonly explained within a
psychogenic framework.
A second limitation is that although we adopted a
systematic search strategy in some sections, in other
sections with fewer studies or wide variations in study
method and design, we used a more narrative approach.
Also, even when we adopted a systematic approach, it
fell short of the full standards required for a compre-
hensive systematic review. For example, we did not
search all possible sources for study reports, nor did we
take into consideration the influence of publication
bias. A third limitation is that, in our review, we did not
address the issue of deliberate feigning. An urgent
future priority is to develop criteria that can be used to
distinguish more effectively between genuine and
feigned illness (see Nicholson, Stone, & Kanaan, 2011,
for discussion).
Conclusion
Given our current limited understanding of medical dis-
ease and its markers, it is perhaps not surprising that not
all physical complaints can be associated with a specific,
well-recognized disease process. In these circumstances,
it is tempting to offer a psychological explanation. How-
ever, in this review, we have argued that such explana-
tions are not currently supported by the evidence, at least
not in the domains considered here. Further, these expla-
nations may be harmful for the patient. To find better
treatments for these illnesses, researchers and practitio-
ners may need to retire those overworked psychological
explanations that are commonly invoked in the face of
uncertainty and instead adopt a completely fresh per-
spective. Such an approach may lead to a much deeper
understanding of this perplexing collection of illnesses.
Declaration of Conflicting Interests
The authors declared that they had no conflicts of interest with
respect to their authorship or the publication of this article.
Supplemental Material
Additional supporting information may be found at http://pps
.sagepub.com/content/by/supplemental-data
Notes
1. If we assume that effect sizes in this domain are relatively
large (Cohen’s d of 0.75 or more), then a study would need
at least to have 30 participants or more in each group to have
sufficient power (.08 or more) to reveal such an effect (Cohen,
1992). Clearly, studies that meet only this minimum requirement
still would be underpowered to reveal smaller effect sizes
2. For an excellent discussion of the potential harms associated
with a psychogenic diagnosis, see Kennedy (2012).
References
Aldao, A., Mennin, D., Linardatos, E., & Fresco, D. M. (2010).
Differential patterns of physical symptoms and subjective
by guest on September 30, 2016pps.sagepub.comDownloaded from
626 Wilshire, Ward
processes in generalized anxiety disorder and unipo-
lar depression. Journal of Anxiety Disorders, 24, 250–259.
doi:10.1016/j.janxdis.2009.12.001
Aldenkamp, A. P., & Mulder, O. (1997). Behavioural mecha-
nisms involved in pseudoepileptic seizures: A comparison
between patients with epileptic seizures and patients with
pseudoepileptic seizures. Seizure, 6, 275–282. doi:10.1016/
S1059-1311(97)80074-X
Alp, M. H., & Grant, A. K. (1970). Personality pattern and emo-
tional stress in the genesis of gastric ulcer. Gut, 11, 773–
777. doi:10.1136/gut.11.9.773
American Psychiatric Association. (2013). Diagnostic and sta-
tistical manual of mental disorders (5th ed.). Washington,
DC: Author.
Anderson, K. E., Gruber-Baldini, A. L., Vaughan, C. G., Reich,
S. G., Fishman, P. S., Weiner, W. J., & Shulman, L. M.
(2007). Impact of psychogenic movement disorders versus
Parkinson’s on disability, quality of life, and psychopathol-
ogy. Movement Disorders, 22, 2204–2209. doi:10.1002/
mds.21687
Arzy, S., Halje, P., Schechter, D. S., Spinelli, L., Seeck, M., &
Blanke, O. (2014). Neural generators of psychogenic sei-
zures: Evidence from intracranial and extracranial brain
recordings. Epilepsy & Behavior, 31, 381–385. doi:10.1016/j
.yebeh.2013.10.017
Bagby, R. M., Parker, J. D., & Taylor, G. J. (1994). The twenty-
item Toronto Alexithymia Scale-I. Item selection and cross-
validation of the factor structure. Journal of Psychosomatic
Research, 38, 23–32. doi:10.1016/0022-3999(94)90005-1
Barnum, R. (2014). Problems with diagnosing conversion
disorder in response to variable and unusual symptoms.
Adolescent Health, Medicine and Therapeutics, 5, 67–71.
doi:10.2147/AHMT.S57486
Barry, E., Krumholz, A., Bergey, G. K., Chatha, H., Alemayehu,
S., & Grattan, L. (1998). Nonepileptic posttraumatic sei-
zures. Epilepsia, 39, 427–431. doi:10.1111/j.1528-1157.1998.
tb01395.x
Barry, J. J., Atzman, O., & Morrell, M. J. (2000). Discriminating
between epileptic and nonepileptic events: The util-
ity of hypnotic seizure induction. Epilepsia, 41, 81–84.
doi:10.1111/j.1528-1157.2000.tb01509.x
Barsky, A. J. (1992). Amplification, somatization, and the somato-
form disorders. Psychosomatics, 33, 28–34. doi:10.1016/
S0033-3182(92)72018-0
Baslet, G. (2011). Psychogenic non-epileptic seizures: A
model of their pathogenic mechanism. Seizure, 20, 1–13.
doi:10.1016/j.seizure.2010.10.032
Bautista, R. E. D., Gonzales-Salazar, W., & Ochoa, J. G. (2008).
Expanding the theory of symptom modeling in patients with
psychogenic nonepileptic seizures. Epilepsy & Behavior, 13,
407–409. doi:10.1016/j.yebeh.2008.04.016
Bazil, C. W., & Walczak, T. S. (1997). Effects of sleep and sleep
stage on epileptic and nonepileptic seizures. Epilepsia, 38,
56–62. doi:10.1111/j.1528-1157.1997.tb01077.x
Beck, A. T. (1961). A systematic investigation of depression.
Comprehensive Psychiatry, 2, 163–170. doi:10.1016/S0010-
440X(61)80020-5
Beck, A. T., Epstein, N., Brown, G., & Steer, R. A. (1988). An
inventory for measuring clinical anxiety: Psychometric
properties. Journal of Consulting and Clinical Psychology,
56, 893–897. doi:10.1037/0022-006X.56.6.893
Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Manual for Beck
Depression Inventory–II. San Antonio, TX: Psychological
Corporation.
Bell, W. L., Park, Y. D., Thompson, E. A., & Radtke, R. A.
(1998). Ictal cognitive assessment of partial seizures and
pseudoseizures. Archives of Neurology, 55, 1456–1459.
doi:10.1001/archneur.55.11.1456
Benbadis, S. R., & Hauser, W. A. (2000). An estimate of the
prevalence of psychogenic non-epileptic seizures. Seizure,
9, 280–281. doi:10.1053/seiz.2000.0409
Bernstein, D. P., Fink, L., Handelsman, L., Foote, J., Lovejoy,
M., Wenzel, K., . . . Ruggiero, J. (1994). Initial reliability and
validity of a new retrospective measure of child abuse and
neglect. American Journal of Psychiatry., 151, 1132–1136.
doi:10.1176/ajp.151.8.1132
Betts, T., & Boden, S. (1992). Diagnosis, management and
prognosis of a group of 128 patients with non-epileptic
attack disorder. Part II. Previous childhood sexual abuse
in the aetiology of these disorders. Seizure, 1, 27–32.
doi:10.1016/1059-1311(92)90050-b
Bodde, N. M., Brooks, J. L., Baker, G. A., Boon, P. A.,
Hendriksen, J. G., & Aldenkamp, A. P. (2009). Psychogenic
non-epileptic seizures—Diagnostic issues: A critical review.
Clinical Neurology & Neurosurgery, 111, 1–9. doi:10.1016/j.
clineuro.2008.09.028
Bodde, N. M., Brooks, J. L., Baker, G. A., Boon, P. A.,
Hendriksen, J. G., Mulder, O. G., & Aldenkamp, A. P.
(2009). Psychogenic non-epileptic seizures—Definition,
etiology, treatment and prognostic issues: A critical review.
Seizure, 18, 543–553. doi:10.1016/j.seizure.2009.06.006
Briere, J. (1992). Methodological issues in the study of sex-
ual abuse effects. Journal of Consulting and Clinical
Psychology, 60, 196–203. doi:10.1037/0022-006X.60.2.196
Brooks, J. L., Goodfellow, L., Bodde, N. M., Aldenkamp, A.,
& Baker, G. A. (2007). Nondrug treatments for psycho-
genic nonepileptic seizures: What’s the evidence? Epilepsy
& Behavior, 11, 367–377. doi:10.1016/j.yebeh.2007.05.007
Brown, R. J. (2004). Psychological mechanisms of medically
unexplained symptoms: An integrative conceptual model.
Psychological Bulletin, 130, 793–812. doi:10.1037/0033-
2909.130.5.793
Brown, R. J. (2005). Dissociation and conversion in psychogenic
illness. In M. Hallett, S. Fahn, & J. Jankovic, et al. (Eds.),
Psychogenic movement disorders: Psychobiology and treat-
ment of a functional disorder (pp. 131–143). Philadelphia,
PA: Lippincott Williams & Wilkins.
Brown, R. J., Syed, T. U., Benbadis, S., LaFrance, W. C., & Reuber,
M. (2011). Psychogenic nonepileptic seizures. Epilepsy &
Behavior, 22, 85–93. doi:10.1016/j.yebeh.2011.02.016
Buxbaum, L. J., Ferraro, M. K., Veramonti, T., Farne, A., Whyte,
J. M. D. P., Ladavas, E., . . . Coslett, H. B. (2004). Hemispatial
neglect subtypes, neuroanatomy, and disability. Neurology,
62, 749–756. doi:10.1212/01.WNL.0000113730.73031.F4
Caplan, L. R., & Nadelson, T. (1980). Multiple sclerosis and
hysteria: Lessons learned from their association. Journal
of the American Medical Association, 243, 2418–2421.
doi:10.1001/jama.1980.03300490036024
by guest on September 30, 2016pps.sagepub.comDownloaded from
Psychogenic Explanations of Illness 627
Carson, A. J., Ringbauer, B., Stone, J., McKenzie, L., Warlow,
C., & Sharpe, M. (2000). Do medically unexplained symp-
toms matter? A prospective cohort study of 300 new refer-
rals to neurology outpatient clinics. Journal of Neurology,
Neurosurgery & Psychiatry, 68, 207–210. doi:10.1136/
jnnp.68.2.207
Cassem, E. H. (1995). Depressive disorders in the medically
ill: An overview. Psychosomatics, 36, S2–S10. doi:10.1016/
S0033-3182(95)71698-X
Chabrol, H., Peresson, G., & Clanet, M. (1995). Lack of spec-
ificity of the traditional criteria for conversion disorders.
European Psychiatry, 10, 317–319. doi:10.1016/0924-
9338(96)80314-2
Chen, D. K., Maheshwari, A., Franks, R., Trolley, G. C., Robinson,
J. S., & Hrachovy, R. A. (2014). Brief group psychoedu-
cation for psychogenic nonepileptic seizures: A neurolo-
gist-initiated program in an epilepsy center. Epilepsia, 55,
156–166. doi:10.1111/epi.12481
Cohen, J. (1992). A power primer. Psychological Bulletin, 112,
155–159. doi:10.1037/0033-2909.112.1.155
Cragar, D. E., Berry, D. T., Fakhoury, T. A., Cibula, J. E.,
& Schmitt, F. A. (2002). A review of diagnostic tech-
niques in the differential diagnosis of epileptic and non-
epileptic seizures. Neuropsychology Review, 12, 31–64.
doi:10.1023/A:1015491123070
Cramer, J. A., Blum, D., Reed, M., & Fanning, K. (2003). The
influence of comorbid depression on quality of life for
people with epilepsy. Epilepsy & Behavior, 4, 515–521.
doi:10.1016/j.yebeh.2003.07.009
Crimlisk, H. L., Bhatia, K., Cope, H., David, A., Marsden, C. D.,
& Ron, M. A. (1998). Slater revisited: Six year follow up
study of patients with medically unexplained motor symp-
toms. British Medical Journal, 316, 582–586. doi:10.1136/
bmj.316.7131.582
Daum, C., Gheorghita, F., Spatola, M., Stojanova, V., Medlin,
F., Vingerhoets, F., . . . Aybek, S. (2015). Interobserver
agreement and validity of bedside “positive signs” for func-
tional weakness, sensory and gait disorders in conversion
disorder: A pilot study. Journal of Neurology, Neurosurgery
& Psychiatry, 86, 425–430. doi:10.1136/jnnp-2013-307381
Davey Smith, G. (2005). The biopsychosocial approach: a note of
caution. In P.D. White (Ed.), Biopsychosocial medicine: An
integrated approach to understanding illness (pp. 77–102).
Oxford, United Kingdom: Oxford University Press.
Davison, P., Sharpe, M., Wade, D., & Bass, C. (1999).
“Wheelchair” patients with nonorganic disease: A psycho-
logical inquiry. Journal of Psychosomatic Research, 47, 93–
103. doi:10.1016/S0022-3999(98)00114-7
Deary, V., Chalder, T., & Sharpe, M. (2007). The cognitive
behavioural model of medically unexplained symptoms:
A theoretical and empirical review. Clinical Psychology
Review, 27, 781–797. doi:10.1016/j.cpr.2007.07.002
Demartini, B., Petrochilos, P., Ricciardi, L., Price, G., Edwards,
M. J., & Joyce, E. (2014). The role of alexithymia in the
development of functional motor symptoms (conversion
disorder). Journal of Neurology, Neurosurgery & Psychiatry,
85, 1132–1137. doi:10.1136/jnnp-2013-307203
Derogatis, L. R. (2000). The Brief Symptom Inventory–18 (BSI-
18): Administration, scoring and procedures manual.
Minneapolis, MN: National Computer Systems.
Derogatis, L. R., & Lipman, R. S. (1977). SCL-90. Administration,
scoring and procedures. Manual-I for the Revised) version
and other instruments of the psychopathology rating scale
series. Baltimore, ML: John Hopkins University School of
Medicine.
Derogatis, L. R., Lipman, R. S., Rickels, K., Uhlenhuth, E. H., &
Covi, L. (1974). The Hopkins Symptom Checklist (HSCL):
A self-report symptom inventory. Behavioral Science, 19,
1–15. doi:10.1002/bs.3830190102
De Ruddere, L., Goubert, L., Stevens, M. A. L., Deveugele, M.,
Craig, K. D., & Crombez, G. (2014). Health care profession-
als’ reactions to patient pain: Impact of knowledge about
medical evidence and psychosocial influences. Journal of
Pain, 15, 262–270. doi:10.1016/j.jpain.2013.11.002
De Ruddere, L., Goubert, L., Stevens, M., Williams, A. C. D. C.,
& Crombez, G. (2013). Discounting pain in the absence of
medical evidence is explained by negative evaluation of the
patient. Pain, 154, 669–676. doi:10.1016/j.pain.2012.12.018
Devinsky, O., Sanchez-Villasenor, F., Vazquez, B., Kothari, M.,
Alper, K., & Luciano, D. (1996). Clinical profile of patients
with epileptic and nonepileptic seizures. Neurology, 46,
1530–1533. doi:10.1212/WNL.46.6.1530
Dohrenwend, B. S., Askenasy, A. R., Krasnoff, L., & Dohrenwend,
B. P. (1978). Exemplification of a method for scaling life
events: The PERI Life Events Scale. Journal of Health and
Social Behavior, 19, 205–229. doi:10.2307/2136536
Edwards, M. J., Adams, R. A., Brown, H., Pareés, I., & Friston,
K. J. (2012). A Bayesian account of “hysteria.” Brain, 135,
3495–3512. doi:10.1093/brain/aws129
Edwards, R. G., Barlow, J. H., & Turner, A. P. (2008). Experiences
of diagnosis and treatment among people with multiple
sclerosis. Journal of Evaluation in Clinical Practice, 14,
460–464. doi:10.1111/j.1365-2753.2007.00902.x
Elliott, J. O., & Charyton, C. (2014). Biopsychosocial predictors
of psychogenic non-epileptic seizures. Epilepsy Research,
108, 1543–1553. doi:10.1016/j.eplepsyres.2014.09.003
Factor, S. A., Podskalny, G. D., & Molho, E. S. (1995).
Psychogenic movement disorders: Frequency, clinical pro-
file, and characteristics. Journal of Neurology, Neurosurgery
& Psychiatry, 59, 406–412. doi:10.1136/jnnp.59.4.406
Fairclough, G., Fox, J., Mercer, G., Reuber, M., & Brown,
R. J. (2014). Understanding the perceived treatment needs
of patients with psychogenic nonepileptic seizures. Epilepsy
& Behavior, 31, 295–303. doi:10.1016/j.yebeh.2013.10.025
Felicio, A. C., Godeiro-Junior, C., Moriyama, T. S., Shih,
M. C., Hoexter, M. Q., Borges, V., . . . Ferraz, H. B.
(2010). Degenerative Parkinsonism in patients with psy-
chogenic Parkinsonism: A dopamine transporter imaging
study. Clinical Neurology & Neurosurgery, 112, 282–285.
doi:10.1016/j.clineuro.2009.12.010
Ferguson, C. J., & Heene, M. (2012). A vast graveyard of undead
theories: Publication bias and psychological science’s aver-
sion to the null. Perspectives on Psychological Science, 7,
555–561. doi:10.1177/1745691612459059
First, M. B., Gibbon, M., Spitzer, R. L., Williams, J. B. W., &
Benjamin, L. S. (1997). Structured clinical interview for
DSM-IV Axis II personality disorders, (SCID-II). Washington,
DC: American Psychiatric Press.
First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. B. W.
(1996). Structured clinical interview for DSM-IV Axis I
by guest on September 30, 2016pps.sagepub.comDownloaded from
628 Wilshire, Ward
disorders: Clinician version (SCID-CV). Washington, DC:
American Psychiatric Press.
Fiszman, A., Alves-Leon, S. V., Nunes, R. G., Isabella, D. A.,
& Figueira, I. (2004). Traumatic events and posttraumatic
stress disorder in patients with psychogenic nonepileptic
seizures: A critical review. Epilepsy & Behavior, 5, 818–825.
doi:10.1016/j.yebeh.2004.09.002
Foy, P. M., Copeland, G. P., & Shaw, M. D. M. (1981). The inci-
dence of postoperative seizures. Acta Neurochirurgica, 55,
253–264. doi:10.1007/BF01808441
Gaitatzis, A., Trimble, M. R., & Sander, J. W. (2004). The psychiat-
ric comorbidity of epilepsy. Acta Neurologica Scandinavica,
110, 207–220. doi:10.1111/j.1600-0404.2004.00324.x
Gelauff, J., Stone, J., Edwards, M., & Carson, A. (2013). The
prognosis of functional (psychogenic) motor symptoms: A
systematic review. Journal of Neurology, Neurosurgery &
Psychiatry, 85, 220–226. doi:jnnp-2013-305321
Glosser, G., Roberts, D., & Glosser, D. S. (1999). Nonepileptic
seizures after resective epilepsy surgery. Epilepsia, 40,
1750–1754. doi:10.1111/j.1528-1157.1999.tb01593.x
Goldstein, L. H., Chalder, T., Chigwedere, C., Khondoker, M. R.,
Moriarty, J., Toone, B. K., & Mellers, J. (2010). Cognitive-
behavioral therapy for psychogenic nonepileptic seizures:
A pilot RCT. Neurology, 74, 1986–1994. doi:10.1212/
WNL.0b013e3181e39658
Goldstein, L. H., Deale, A. C., O’Malley, S. J., Toone, B., &
Mellers, J. (2004). An evaluation of cognitive behavioral
therapy as a treatment for dissociative seizures: A pilot
study. Cognitive and Behavioral Neurology, 17, 41–49.
doi:10.1097/00146965-200403000-00005
Gosselin, N., Bottari, C., Chen, J. K., Petrides, M., Tinawi, S., de
Guise, É., & Ptito, A. (2011). Electrophysiology and func-
tional MRI in post-acute mild traumatic brain injury. Journal
of Neurotrauma, 28, 329–341. doi:10.1089/neu.2010.1493
Gould, R., Miller, B. L., Goldberg, M. A., & Benson, D. F.
(1986). The validity of hysterical signs and symptoms.
The Journal of Nervous and Mental Disease, 174, 593–597.
doi:10.1097/00005053-198610000-00003
Grabowska-Grzyb, A., Je˛ drzejczak, J., Nagan´ska, E., & Fiszer,
U. (2006). Risk factors for depression in patients with
epilepsy. Epilepsy & Behavior, 8, 411–417. doi:10.1016/j
.yebeh.2005.12.005
Greenberg, S. A. (2009). How citation distortions create
unfounded authority: Analysis of a citation network. British
Medical Journal, 339, Article b2680. doi:10.1136/bmj.b2680
Gröppel, G., Kapitany, T., & Baumgartner, C. (2000).
Cluster analysis of clinical seizure semiology of psy-
chogenic nonepileptic seizures. Epilepsia, 41, 610–614.
doi:10.1111/j.1528-1157.2000.tb00216.x
Gupta, A., & Lang, A. E. (2009). Psychogenic movement dis-
orders. Current Opinion in Neurology, 22, 430–436.
doi:10.1097/WCO.0b013e32832dc169
Guthrie, T. C., & Nelson, D. A. (1995). Influence of temperature
changes on multiple sclerosis: Critical review of mechanisms
and research potential. Journal of the Neurological Sciences,
129, 1–8. doi:10.1016/0022-510X(94)00248-M
Harden, C. L., Burgut, F., & Kanner, A. M. (2003). The diag-
nostic significance of video EEG monitoring findings on
pseudoseizure patients differs between neurologists and
psychiatrists. Epilepsia, 44, 453–456. doi:10.1046/j.1528-
1157.2003.33002.x
Hinson, V. K., Weinstein, S., Bernard, B., Leurgans, S. E., &
Goetz, C. G. (2006). Single-blind clinical trial of psycho-
therapy for treatment of psychogenic movement disor-
ders. Parkinsonism & Related Disorders, 12, 177–180.
doi:10.1016/j.parkreldis.2005.10.006
Holmes, T. H., & Rahe, R. H. (1967). The Social Readjustment
Rating Scale. Journal of Psychosomatic Research, 11, 213–
218. doi:10.1016/0022-3999(67)90010-4
Hotopf, M. (2004). Preventing somatization. Psychological
Medicine, 34, 195–198. doi:10.1017/S003329170300151X
Hovorka, J., Nežádal, T., Herman, E., Neˇmcová, I., & Bajacˇek,
M. (2007). Psychogenic non-epileptic seizures, prospective
clinical experience: Diagnosis, clinical features, risk fac-
tors, psychiatric comorbidity, treatment outcome. Epileptic
Disorders, 9(5), 52–58.
Hubsch, C., Baumann, C., Hingray, C., Gospodaru, N., Vignal,
J. P., Vespignani, H., & Maillard, L. (2011). Clinical clas-
sification of psychogenic non-epileptic seizures based
on video EEG analysis and automatic clustering. Journal
of Neurology, Neurosurgery & Psychiatry, 82, 955–960.
doi:10.1136/jnnp.2010.235424
Hudak, A. M., Trivedi, K., Harper, C. R., Booker, K., Caesar,
R. R., Agostini, M., . . . Diaz-Arrastia, R. (2004). Evaluation
of seizure-like episodes in survivors of moderate and
severe traumatic brain injury. Journal of Head Trauma
Rehabilitation, 19, 290–295. doi:10.1097/00001199-
200407000-00003
Ioannidis, J. P. (2012). Why science is not necessarily self-
correcting. Perspectives on Psychological Science, 7, 645–
654. doi:10.1177/1745691612464056
Jannot, A. S., Agoritsas, T., Gayet-Ageron, A., & Perneger,
T. V. (2013). Citation bias favoring statistically signifi-
cant studies was present in medical research. Journal
of Clinical Epidemiology, 66, 296–301. doi:10.1016/j
.jclinepi.2012.09.015
Jüni, P., Altman, D. G., & Egger, M. (2001). Assessing the qual-
ity of controlled clinical trials. British Medical Journal, 323,
42–46. doi:10.1136/bmj.323.7303.42
Karterud, H. N., Knizek, B. L., & Nakken, K. O. (2010). Changing
the diagnosis from epilepsy to PNES: Patients’ experiences
and understanding of their new diagnosis. Seizure, 19, 40–
46. doi:10.1016/j.seizure.2009.11.001
Katon, W. J. (2003). Clinical and health services relationships
between major depression, depressive symptoms, and gen-
eral medical illness. Biological Psychiatry, 54, 216–226.
doi:10.1016/S0006-3223(03)00273-7
Kennedy, A. (2012). Authors of our own misfortune: The prob-
lems with psychogenic explanations for physical illnesses.
South Willingham, England: Village Digital Press.
Kenney, C., Diamond, A., Mejia, N., Davidson, A., Hunter,
C., & Jankovic, J. (2007). Distinguishing psychogenic and
essential tremor. Journal of the Neurological Sciences, 263,
94–99. doi:10.1016/j.jns.2007.06.008
Khan, A., Baade, L., Ablah, E., McNerney, V., Golewale, M., &
Liow, K. (2009). Can hypnosis differentiate epileptic from
by guest on September 30, 2016pps.sagepub.comDownloaded from
Psychogenic Explanations of Illness 629
nonepileptic events in the video/EEG monitoring unit?
Data from a pilot study. Epilepsy & Behavior, 15, 314–317.
doi:10.1016/j.yebeh.2009.04.004
Kimiskidis, V. K., Triantafyllou, N. I., Kararizou, E., Gatzonis,
S. S., Fountoulakis, K. N., Siatouni, A., . . . Kaprinis, G. S.
(2007). Depression and anxiety in epilepsy: The association
with demographic and seizure-related variables. Annals
of General Psychiatry, 6(1), Article 28. doi:10.1186/1744-
859X-6-28
King, N. S. (2003). Post-concussion syndrome: Clarity amid the
controversy? British Journal of Psychiatry, 183, 276–278.
doi:10.1192/bjp.183.4.276
Kisely, S., Goldberg, D., & Simon, G. (1997). A comparison
between somatic symptoms with and without clear organic
cause: Results of an international study. Psychological
Medicine, 27, 1011–1019. doi:10.1017/S0033291797005485
Kole, A., & Faurisson, F. (2009). The voice of 12,000 patients:
Experiences and expectations of rare disease patients
on diagnosis and care in Europe. Retrieved from http://
www.eurordis.org/IMG/pdf/voice_12000_patients/
EURORDISCARE_FULLBOOKr.pdf
Kompoliti, K., Wilson, B., Stebbins, G., Bernard, B., & Hinson,
V. (2014). Immediate vs. delayed treatment of psycho-
genic movement disorders with short term psychodynamic
psychotherapy: Randomized clinical trial. Parkinsonism
& Related Disorders, 20, 60–63. doi:10.1016/j.parkrel-
dis.2013.09.018
Kranick, S., Ekanayake, V., Martinez, V., Ameli, R., Hallett,
M., & Voon, V. (2011). Psychopathology and psychogenic
movement disorders. Movement Disorders, 26, 1844–1850.
doi:10.1002/mds.23830
Kroenke, K., Spitzer, R., Williams, J., Linzer, M., Hahn, S.,
deGruy, F., III, & Brody, D. (1994). Physical symptoms in
primary care: Predictors of psychiatric disorders and func-
tional impairment. Archives of Family Medicine, 3, 774–779.
doi:10.1001/archfami.3.9.774
Kubany, E. S., Leisen, M. B., Kaplan, A. S., Watson, S. B., Haynes,
S. N., Owens, J. A., & Burns, K. (2000). Development and
preliminary validation of a brief broad-spectrum measure of
trauma exposure: The Traumatic Life Events Questionnaire.
Psychological Assessment, 12, 210–224. doi:10.1037/1040-
3590.12.2.210
LaFrance, W. C., Baird, G. L., Barry, J. J., Blum, A. S., Webb,
A. F., Keitner, G. I., . . . Szaflarski, J. P. (2014). Multicenter
pilot treatment trial for psychogenic nonepileptic seizures:
A randomized clinical trial. JAMA Psychiatry, 71, 997–1005.
doi:10.1001/jamapsychiatry.2014.817
LaFrance, W. C., Miller, I. W., Ryan, C. E., Blum, A. S., Solomon,
D. A., Kelley, J. E., & Keitner, G. I. (2009). Cognitive behav-
ioral therapy for psychogenic nonepileptic seizures. Epilepsy
& Behavior, 14, 591–596. doi:10.1016/j.yebeh.2009.02.016
Landers, M., Wulf, G., Wallmann, H., & Guadagnoli, M. (2005).
An external focus of attention attenuates balance impair-
ment in patients with Parkinson’s disease who have a
fall history. Physiotherapy, 91, 152–158. doi:10.1016/j
.physio.2004.11.010
Lang, A. E., Koller, W. C., & Fahn, S. (1995). Psychogenic par-
kinsonism. Archives of Neurology, 52, 802–810. doi:10.1001/
archneur.1995.00540320078015
Langworthy, O. R. (1948). Relation of personality problems
to onset and progress of multiple sclerosis. Archives of
Neurology & Psychiatry, 59, 13–28. doi:10.1001/archneur-
psyc.1948.02300360023002
Lempert, T., Dieterich, M., Huppert, D., & Brandt, T. (1990).
Psychogenic disorders in neurology: Frequency and clini-
cal spectrum. Acta Neurologica Scandinavica, 82, 335–340.
doi:10.1111/j.1600-0404.1990.tb03312.x
Lempert, T., & Schmidt, D. (1990). Natural history and outcome
of psychogenic seizures: A clinical study in 50 patients.
Journal of Neurology, 237, 35–38. doi:10.1007/BF00319665
Lipowski, Z. J. (1988). Somatization: The concept and its clini-
cal application. American Journal of Psychiatry, 145, 1358–
1368. doi:10.1176/ajp.145.11.1358
Martlew, J., Pulman, J., & Marson, A. G. (2014). Psychological and
behavioural treatments for adults with non-epileptic attack
disorder. Cochrane Database of Systematic Reviews, Issue 2,
Art. No. CD006370. doi:10.1002/14651858.CD006370.pub2
Mayor, R., Howlett, S., Grünewald, R., & Reuber, M.
(2010). Long-term outcome of brief augmented psy-
chodynamic interpersonal therapy for psychogenic
nonepileptic seizures. Epilepsia, 51, 1169–1176. doi:10.1111/
j.1528-1167.2010.02656.x
McClary, A. R., Meyer, E., & Weitzman, E. L. (1955). Observations
on the role of the mechanism of depression in some patients
with disseminated lupus erythematosus. Psychosomatic
Medicine, 17, 311–321. doi:10.1097/00006842-195507000-
00006
McKegney, P. F., Gordon, R. O., & Levine, S. M. (1970). A psy-
chosomatic comparison of patients with ulcerative colitis
and Crohn’s disease. Psychosomatic Medicine, 32, 153–166.
doi:10.1097/00006842-197003000-00003
McLaughlin, D. P., & McFarland, K. (2011). A randomized trial
of a group based cognitive behavior therapy program for
older adults with epilepsy: The impact on seizure frequency,
depression and psychosocial well-being. Journal of Behavioral
Medicine, 34, 201–207. doi:10.1007/s10865-010-9299-z
Merckelbach, H., & Muris, P. (2001). The causal link between
self-reported trauma and dissociation: A critical review.
Behaviour Research and Therapy, 39, 245–254. doi:10.1016/
S0005-7967(99)00181-3
Mildon, B. (2015, April 15). Turning patients into numbers.
Retrieved from http://www.madinamerica.com/2015/04/
turning-patients-numbers/
Moene, F. C., Landberg, E. H., Hoogduin, K. A., Spinhoven,
P., Hertzberger, L. I., Kleyweg, R. P., & Weeda, J. (2000).
Organic syndromes diagnosed as conversion disorder:
Identification and frequency in a study of 85 patients.
Journal of Psychosomatic Research, 49, 7–12. doi:10.1016/
S0022-3999(99)00107-5
Moene, F. C., Spinhoven, P., Hoogduin, K. A., & van Dyck,
R. (2002). A randomised controlled clinical trial on the
additional effect of hypnosis in a comprehensive treatment
programme for in-patients with conversion disorder of the
motor type. Psychotherapy and Psychosomatics, 71, 66–76.
doi:10.1159/000049348
Montgomery, S. A., & Asberg, M. (1979). A new depression
scale designed to be sensitive to change. British Journal of
Psychiatry, 134, 382–389. doi:10.1192/bjp.134.4.382
by guest on September 30, 2016pps.sagepub.comDownloaded from
630 Wilshire, Ward
Montori, V. M., & Guyatt, G. H. (2001). Intention-to-treat princi-
ple. Canadian Medical Association Journal, 165, 1339–1341.
Moos, R. H. (1964). Personality factors associated with rheu-
matoid arthritis: A review. Journal of Chronic Diseases, 17,
41–55. doi:10.1016/0021-9681(64)90038-4
Moos, R. H. (1974). Family Environment Scale (Form R). Palo
Alto, CA: Consulting Psychologists Press.
Morgante, F., Edwards, M. J., Espay, A. J., Fasano, A., Mir, P., &
Martino, D. (2012). Diagnostic agreement in patients with
psychogenic movement disorders. Movement Disorders, 27,
548–552. doi:10.1002/mds.24903
Nettleton, S., Watt, I., O'Malley, L., & Duffey, P. (2005).
Understanding the narratives of people who live with
medically unexplained illness. Patient Education and
Counseling, 56, 205–210. doi:10.1016/j.pec.2004.02.010
Nicholson, T. R., Stone, J., & Kanaan, R. A. (2011). Conversion
disorder: A problematic diagnosis. Journal of Neurology,
Neurosurgery & Psychiatry, 82, 1267–1273. doi:10.1136/
jnnp.2008.171306
Nijenhuis, E. R. (2001). Somatoform dissociation: Major symp-
toms of dissociative disorders. Journal of Trauma &
Dissociation, 1, 7–32. doi:10.1300/J229v01n04_02
Nuti, A., Ceravolo, R., Piccinni, A., Dell’Agnello, G., Bellini,
G., Gambaccini, G., . . . Bonuccelli, U. (2004). Psychiatric
comorbidity in a population of Parkinson’s disease patients.
European Journal of Neurology, 11, 315–320. doi:10.1111/
j.1468-1331.2004.00781.x
Oliva, M., Pattison, C., Carino, J., Roten, A., Matkovic, Z., &
O’Brien, T. J. (2008). The diagnostic value of oral lacerations
and incontinence during convulsive “seizures.” Epilepsia,
49, 962–967. doi:10.1111/j.1528-1167.2008.01554.x
Orbach, D., Ritaccio, A., & Devinsky, O. (2003). Psychogenic, non-
epileptic seizures associated with video-EEG verified sleep.
Epilepsia, 44, 64–68. doi:10.1046/j.1528-1157.2003.29302.x
Pareés, I., Kojovic, M., Pires, C., Rubio-Agusti, I., Saifee, T. A., Sadnicka,
A., . . . Edwards, M. J. (2014). Physical precipitating factors in
functional movement disorders. Journal of the Neurological
Sciences, 338, 174–177. doi:10.1016/j.jns.2013.12.046
Pareés, I., Saifee, T. A., Kojovic, M., Kassavetis, P., Rubio-Agusti,
I., Sadnicka, A., . . . Edwards, M. J. (2013). Functional (psy-
chogenic) symptoms in Parkinson’s disease. Movement
Disorders, 28, 1622–1627. doi:10.1002/mds.25544
Parker, G., Tupling, H., & Brown, L. (1979). A parental bonding
instrument. British Journal of Medical Psychology, 52, 1–10.
doi:10.1111/j.2044-8341.1979.tb02487.x
Parra, J., Iriarte, J., & Kanner, A. M. (1999). Are we overusing
the diagnosis of psychogenic non-epileptic events? Seizure,
8, 223–227. doi:10.1053/seiz.1999.0285
Pillai, J. A., & Haut, S. R. (2012). Patients with epilepsy and
psychogenic non-epileptic seizures: An inpatient video-
EEG monitoring study. Seizure, 21, 24–27. doi:10.1016/j
.seizure.2011.09.002
Pillai, J. A., Haut, S. R., & Masur, D. (2015). Orbitofrontal cor-
tex dysfunction in psychogenic non-epileptic seizures. A
proposal for a two-factor model. Medical Hypotheses, 84,
363–369. doi:10.1016/j.mehy.2015.01.034
Pope, H. G., & Hudson, J. I. (1995). Does childhood sexual
abuse cause adult psychiatric disorders? Essentials of meth-
odology. Journal of Psychiatry & Law, 23, 363–381.
Prigatano, G. P., Stonnington, C. M., & Fisher, R. S. (2002).
Psychological factors in the genesis and management of
nonepileptic seizures: Clinical observations. Epilepsy &
Behavior, 3, 343–349. doi:10.1016/S1525-5050(02)00053-7
Ranawaya, R., Riley, D., & Lang, A. (1990). Psychogenic dyskinesias
in patients with organic movement disorders. Movement
Disorders, 5, 127–133. doi:10.1002/mds.870050206
Reuber, M. (2009). The etiology of psychogenic non-epileptic
seizures: Toward a biopsychosocial model. Neurologic
Clinics, 27, 909–924. doi:10.1016/j.ncl.2009.06.004
Reuber, M., Fernández, G., Bauer, J., Singh, D. D., & Elger,
C. E. (2002). Interictal EEG abnormalities in patients with
psychogenic nonepileptic seizures. Epilepsia, 43, 1013–
1020. doi:10.1046/j.1528-1157.2002.52301.x
Reuber, M., Fernandez, G., Helmstaedter, C., Qurishi, A.,
& Elger, C. E. (2002). Evidence of brain abnormality in
patients with psychogenic nonepileptic seizures. Epilepsy &
Behavior, 3, 249–254. doi:10.1016/S1525-5050(02)00004-5
Reuber, M., Kral, T., Kurthen, M., & Elger, C. E. (2002). New-
onset psychogenic seizures after intracranial neurosurgery.
Acta Neurochirurgica, 144, 901–907. doi:10.1007/s00701-
002-0993-7
Riemann, D., & Voderholzer, U. (2003). Primary insomnia:
A risk factor to develop depression? Journal of Affective
Disorders, 76, 255–259.
Rind, B., Tromovitch, P., & Bauserman, R. (1998). A meta-
analytic examination of assumed properties of child sexual
abuse using college samples. Psychological Bulletin, 124,
22–53. doi:10.1037/0033-2909.124.1.22
Ruddy, R., & House, A. (2005). Psychosocial interventions for
conversion disorder. Cochrane Database of Systematic
Reviews, Issue 4, Art. No. CD005331. doi:10.1002/14651858.
CD005331.pub2
Salmon, P., Al-Marzooqi, S. M., Baker, G., & Reilly, J. (2003).
Childhood family dysfunction and associated abuse in
patients with nonepileptic seizures: Towards a causal model.
Psychosomatic Medicine, 65, 695–700. doi:10.1097/01.
PSY.0000075976.20244.D8
Sauseng, P., Klimesch, W., Schabus, M., & Doppelmayr, M.
(2005). Fronto-parietal EEG coherence in theta and upper
alpha reflect central executive functions of working mem-
ory. International Journal of Psychophysiology, 57, 97–103.
doi:10.1016/j.ijpsycho.2005.03.018
Saygi, S., Katz, A., Marks, D. A., & Spencer, S. S. (1992). Frontal
lobe partial seizures and psychogenic seizures Comparison
of clinical and ictal characteristics. Neurology, 42, 1274–
1277. doi:10.1212/WNL.42.7.1274
Scévola, L., Teitelbaum, J., Oddo, S., Centurión, E., Loidl,
C. F., & Kochen, S. (2013). Psychiatric disorders in patients
with psychogenic nonepileptic seizures and drug-resistant
epilepsy. Epilepsy & Behavior, 29, 155–160. doi:10.1016/j
.yebeh.2013.07.012
Sharpe, D., & Faye, C. (2006). Non-epileptic seizures and
child sexual abuse: A critical review of the literature.
Clinical Psychology Review, 26, 1020–1040. doi:10.1016/j
.cpr.2005.11.011
Shenton, M. E., Hamoda, H. M., Schneiderman, J. S., Bouix, S.,
Pasternak, O., Rathi, Y., . . . Zafonte, R. (2012). A review of
magnetic resonance imaging and diffusion tensor imaging
by guest on September 30, 2016pps.sagepub.comDownloaded from
Psychogenic Explanations of Illness 631
findings in mild traumatic brain injury. Brain Imaging and
Behavior, 6, 137–192. doi:10.1007/s11682-012-9156-5
Sierra, M., & Berrios, G. E. (1999). Towards a neuropsychiatry
of conversive hysteria. Cognitive Neuropsychiatry, 4, 267–
287. doi:10.1080/135468099395963
Simmons, J. P., Nelson, L. D., & Simonsohn, U. (2011).
False-positive psychology undisclosed flexibility in
data collection and analysis allows presenting anything
as significant. Psychological Science, 22, 1359–1366.
doi:10.1177/0956797611417632
Slater, E. T., & Glithero, E. (1965). A follow-up of patients diag-
nosed as suffering from “hysteria.” Journal of Psychosomatic
Research, 9, 9–13. doi:10.1016/0022-3999(65)90004-8
Slater, J. D., Brown, M. C., Jacobs, W., & Ramsay, R. E. (1995).
Induction of pseudoseizures with intravenous saline pla-
cebo. Epilepsia, 36, 580–585. doi:10.1111/j.1528-1157.1995.
tb02571.x
Solvason, H. B., Harris, B., Zeifert, P., Flores, B. H., & Hayward,
C. (2002). Psychological versus biological clinical interpre-
tation: A patient with prion disease. American Journal of
Psychiatry, 159, 528–537. doi:10.1176/appi.ajp.159.4.528
Spector, S., Cull, C., & Goldstein, L. H. (2000). Seizure precipi-
tants and perceived self-control of seizures in adults with
poorly-controlled epilepsy. Epilepsy Research, 38, 207–216.
doi:10.1016/S0920-1211(99)00093-5
Spitzer, C., Spelsberg, B., Grabe, H. J., Mundt, B., & Freyberger,
H. J. (1999). Dissociative experiences and psychopathol-
ogy in conversion disorders. Journal of Psychosomatic
Research, 46, 291–294. doi:10.1016/S0022-3999(98)00112-3
Staines, G. L., & Cleland, C. M. (2007). Bias in meta-analytic
estimates of the absolute efficacy of psychotherapy. Review
of General Psychology, 11, 329–347. doi:10.1037/1089-
2680.11.4.329
Stone, J., Carson, A., Aditya, H., Prescott, R., Zaubi, M., Warlow,
C., & Sharpe, M. (2009). The role of physical injury in motor
and sensory conversion symptoms: A systematic and nar-
rative review. Journal of Psychosomatic Research, 66, 383–
390. doi:10.1016/j.jpsychores.2008.07.010
Stone, J., Smyth, R., Carson, A., Lewis, S., Prescott, R., Warlow,
C., & Sharpe, M. (2005). Systematic review of misdiagno-
sis of conversion symptoms and “hysteria.” British Medical
Journal, 331, Article 989. doi:10.1136/bmj.38628.466898.55
Syed, T. U., LaFrance, W. C., Kahriman, E. S., Hasan, S. N.,
Rajasekaran, V., Gulati, D., . . . Pawlowski, M. (2011).
Can semiology predict psychogenic nonepileptic seizures?
A prospective study. Annals of Neurology, 69, 997–1004.
doi:10.1002/ana.22345
Tang, V., Michaelis, R., & Kwan, P. (2014). Psychobehavioral
therapy for epilepsy. Epilepsy & Behavior, 32, 147–155.
doi:10.1016/j.yebeh.2013.12.004
Taylor, G. J., Bagby, R. M., & Parker, J. D. (1991). The alexi-
thymia construct: A potential paradigm for psychosomatic
medicine. Psychosomatics, 32, 153–164. doi:10.1016/S0033-
3182(91)72086-0
Testa, S. M., Krauss, G. L., Lesser, R. P., & Brandt, J. (2012).
Stressful life event appraisal and coping in patients with
psychogenic seizures and those with epilepsy. Seizure, 21,
282–287. doi:10.1016/j.seizure.2012.02.002
van Hilten, J. J., Geraedts, E. J., & Marinus, J. (2007). Peripheral
trauma and movement disorders. Parkinsonism &
Related Disorders, 13, S395–S399. doi:10.1016/s1353-
8020(08)70037-3
van Merode, T., Twellaar, M., Kotsopoulos, I. A. W., Kessels, A.
G. H., Merckelbach, H., de Krom, M. C., & Knottnerus, J. A.
(2004). Psychological characteristics of patients with newly
developed psychogenic seizures. Journal of Neurology,
Neurosurgery & Psychiatry, 75, 1175–1177. doi:10.1136/
jnnp.2003.016923
Voon, V., Brezing, C., Gallea, C., & Hallett, M. (2011). Aberrant
supplementary motor complex and limbic activity during
motor preparation in motor conversion disorder. Movement
Disorders, 26, 2396–2403. doi:10.1002/mds.23890
Vossler, D. G. (1995). Nonepileptic seizures of physiologic origin.
Journal of Epilepsy, 8, 1–10. doi:10.1016/0896-6974(94)00014-Q
Vuilleumier, P., Chicherio, C., Assal, F., Schwartz, S., Slosman,
D., & Landis, T. (2001). Functional neuroanatomical cor-
relates of hysterical sensorimotor loss. Brain, 124, 1077–
1090. doi:10.1093/brain/124.6.1077
Walczak, T. S., Williams, D. T., & Berten, W. (1994). Utility and
reliability of placebo infusion in the evaluation of patients
with seizures. Neurology, 44, 394. doi:10.1212/WNL.44.3_
Part_1.394
Ward, L. C. (2006). Comparison of factor structure models for
the Beck Depression Inventory-II. Psychological Assessment,
18, 81–88. doi:10.1037/1040-3590.18.1.81
Westbrook, L. E., Devinsky, O., & Geocadin, R. (1998).
Nonepileptic seizures after head injury. Epilepsia, 39, 978–
982. doi:10.1111/j.1528-1157.1998.tb01447.x
Wiener, A. (1992). The Dissociative Experiences Scale.
American Journal of Psychiatry, 149, 143–144. doi:10.1176/
ajp.149.1.143-a
Woodward, J. (2007). Interventionist theories of causation in
psychological perspective. In A. Gopnik & L. Schulz (Eds.),
Causal learning: Psychology, philosophy, and computation
(pp. 19–36). Oxford, England: Oxford University Press.
Zaidi, A., Clough, P., Cooper, P., Scheepers, B., & Fitzpatrick,
A. P. (2000). Misdiagnosis of epilepsy: Many seizure-
like attacks have a cardiovascular cause. Journal of the
American College of Cardiology, 36, 181–184. doi:10.1016/
S0735-1097(00)00700-2
by guest on September 30, 2016pps.sagepub.comDownloaded from
... While a precipitating stressor may be identified, this is not a requirement for diagnosis. This is due to recent research that has demonstrated that only about one-third of patients diagnosed with FNSD have a history of trauma (Roelofs & Spinhoven, 2007), and there is little evidence of a psychiatric diagnosis to explain patients' symptoms (Crimlisk et al., 1998;Wilshire & Ward, 2016). In a study of pediatric patients with FNSD presenting to the ED, 25% denied even mundane stressors and all denied history of sexual abuse or trauma (de Gusmao et al., 2014). ...
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