Psychological Bulletin Copyright 2004 by the American Psychological Association

2004, Vol. 130, No. 5, 793– 812 0033-2909/04/$12.00 DOI: 10.1037/0033-2909.130.5.793

Psychological Mechanisms of Medically Unexplained Symptoms:

An Integrative Conceptual Model

Richard J. Brown
University of Manchester and Institute of Neurology

Theories of medically unexplained illness based on the concepts of dissociation, conversion, and
somatization are summarized. Evidence cited in support of these theories is described and the conceptual
strengths and shortcomings of each approach are considered. It is argued that each of these approaches
adds to the understanding of unexplained illness but that none is able to provide a comprehensive
explanation of the phenomenon. An integrative conceptual model of unexplained illness based on
cognitive psychological principles is then presented. This model attempts to combine existing theoretical
approaches within a single explanatory framework, extending previous theory by explaining how
compelling symptoms can exist in the absence of organic pathology. The clinical and empirical
implications of the model are then considered.

Throughout history, medical practitioners have encountered in-
dividuals with symptoms of physical illness for which no adequate
organic basis can be found. According to some estimates, between
25% and 60% of the symptoms investigated in family medical
centers defy adequate physical explanation (Kirkwood et al.,
1982). In some cases, symptoms represent the somatic component
of a diagnosable psychiatric condition, such as anxiety or depres-
sion, but are not recognized as such by the patient or the physician;
in others, normal bodily sensations or minor physical ailments may
be perceived as evidence of serious underlying pathology by a
hypochondriacal individual. In many cases, however, there is no
obvious psychiatric explanation for the symptoms in question
(Kroenke & Swindle, 2000). Although many such “medically
unexplained” symptoms resolve quickly and spontaneously, symp-
toms often remain unresolved, causing distress and disability that
persists over time. In addition to the suffering and uncertainty
faced by patients in this context, the cost of repeated consultation
and investigation for these individuals represents a considerable
burden to the health care services. This is particularly true in the
case of individuals who experience and seek help for multiple
unexplained symptoms, for whom health care costs may be up to
nine times the primary care average (G. R. Smith, Monson, & Ray,
1986).
The psychological origin of medically unexplained symptoms
has been widely recognized since the 18th century (Merskey,
1979), and a number of models attempting to explain these phe-
Richard J. Brown, Academic Division of Clinical Psychology, Univer-
sity of Manchester, Manchester, United Kingdom, and Department of
Clinical Epilepsy, Institute of Neurology, London, United Kingdom.
I thank Chris Frith, Francesca Happé, David Oakley, Karin Roelofs,
Maria Ron, Michael Trimble, and particularly Amanda Barnier for reading
and commenting on earlier versions of this article.
Correspondence concerning this article should be addressed to Richard
J. Brown, Academic Division of Clinical Psychology, University of
Manchester, Second Floor Research and Education Block, Wythenshawe
Hospital, Manchester M23 9LT, United Kingdom. E-mail:
richardjamesbrown@hotmail.com
nomena have been advanced since this time. This article provides
a critical review of the different theories purporting to explain the
pathogenesis of medically unexplained symptoms, considering
both the merits and the limitations of current ideas in this area. On
the basis of this review, I argue that (a) different theories are able
to account for certain features of medically unexplained illness, but
no one theory can accommodate all of the available evidence
concerning these conditions, and that (b) no theory provides a
satisfactory account of how apparently compelling symptoms can
exist in the absence of significant organic pathology. I then de-
scribe a novel model that aims to address these shortcomings by
reference to contemporary cognitive psychological research.
Rather than superceding existing theories in this area, this model
has been developed with a view to integrating current theoretical
concepts within a single explanatory framework. This framework
provides a useful tool to organize available research and theory
concerning medically unexplained symptoms and allows for the
generation of new hypotheses concerning these phenomena.
Background
Classification
Broadly speaking, the fourth edition of the Diagnostic and
Statistical Manual of Mental Disorders (DSM–IV; American Psy-
chiatric Association, 1994) categorizes medically unexplained
complaints according to the nature, number, and duration of the
symptoms in question. The somatoform disorders category encom-
passes a range of complaints characterized by the symptoms of
somatic illness (e.g., pain, fatigue, general malaise) that cannot be
accounted for by identifiable physical pathology, including the
contemporary manifestation of polysymptomatic hysteria (“Bri-
quet’s syndrome”), so-called somatization disorder. The conver-
sion disorders category, a subcategory of the somatoform disor-
ders, encompasses unexplained symptoms suggestive of a
neurological condition, such as gait disturbances, convulsions,
sensory loss, and cognitive decline; symptoms specifically involv-
ing a disruption of memory, perception, and identity are classified

793
794 BROWN
as dissociative disorders, as are the phenomena of depersonaliza-
tion and derealization. DSM–IV also identifies hypochondriasis
and body dysmorphic disorder as somatoform phenomena; neither
of these conditions has medically unexplained symptoms as a
defining feature, and they are not considered in any detail here.
In all cases, symptoms are classified as medically unexplained if
adequate investigation has failed to identify a plausible physical
cause for their occurrence or their associated level of impairment;
they must also cause clinically significant functional disability or
distress to meet diagnostic criteria. Moreover, the symptoms can-
not be solely attributable to diagnosable anxiety, depression, hy-
pochondriasis, or psychosis.
Epidemiology
Unexplained symptoms are ubiquitous, representing the com-
monest single category of complaints encountered in primary care
(Kirmayer & Taillefer, 1997). Evidence suggests that more than a
quarter of unselected primary care patients meet criteria for
DSM–IV undifferentiated somatoform disorder, defined as the
presence of one or more debilitating unexplained symptom of at
least 6 months duration (Fink, Sørensen, Engberg, Holm, & Munk-
Jørgensen, 1999). Patients with a history of multiple unexplained
symptoms are also extremely common. Data reported by Escobar,
Waitzkin, Cohen Silver, Gara, and Holman (1998), for example,
indicate that 22% of primary care patients meet criteria for the
so-called abridged somatization construct, defined as the lifetime
occurrence of four unexplained symptoms in men, six in women.
Many patients with a history of multiple unexplained symptoms
report experiencing several symptoms simultaneously. Kroenke et
al. (1997), for example, presented data indicating that more than
8% of unselected primary care patients meet criteria for so-called
multisomatoform disorder, defined as the presence of three or
more currently distressing unexplained symptoms alongside a his-
tory of somatoform illness.
Research investigating the epidemiology of conversion disorder
has typically used specialist populations, and consequently, little is
known about its primary care prevalence. Mace and Trimble
(1996) suggested that as many as 20% of specialist neurological
patients present with symptoms that defy adequate organic expla-
nation (for a review, see Akagi & House, 2001).
Clinical Features
The most commonly observed unexplained symptoms in pri-
mary care are pain, fatigue, and general malaise (Kirkwood et al.,
1982), although gastrointestinal and sexual/reproductive symp-
toms are frequently found. Within neurological settings, both
“negative” (i.e., those characterized by a loss of normal function-
ing; e.g., sensory loss, amnesia, paralysis, nonconvulsive pseudo-
seizures) and “positive” symptoms (i.e., those characterized by the
presence of additional symptoms that disrupt functioning; e.g., gait
disturbance, tremor, pseudohallucinations, convulsive pseudosei-
zures) are common. Broadly speaking, the most common somato-
form phenomena involve a significant subjective component (e.g.,
pain, fatigue, dizziness) or involve a disruption in the voluntary
control of action (e.g., gait disturbance, urinary retention, dyspha-
gia). Unexplained symptoms are significantly more common in
women than in men, although the phenomenon is no longer con-
sidered an exclusively female problem.
Diagnosis
Distinguishing somatoform symptoms from their organic coun-
terparts can be extremely difficult and typically requires extensive
physical investigation before a firm diagnosis can be made (see,
e.g., Brown & Ron, 2002; Brown & Trimble, 2000). In a small
proportion of cases, symptoms are physiologically impossible
(e.g., triple vision); in others, a somatoform or dissociative diag-
nosis may be suspected because of the variability or medical
implausibility of the symptom in question. In cases of conversion
aphonia, for example, the patient may have a preserved ability to
cough (requiring intact vocal chord function) despite being unable
to speak or whisper. Similarly, unexplained sensory loss is often
inconsistent with actual patterns of sensory innervation (e.g., as in
“glove” and “stocking” anesthesia in the absence of neuropathy).
Although the validity of making a firm diagnosis of unexplained
illness has been questioned over the years (e.g., Slater & Glitherco,
1965), recent research by Crimlisk et al. (1998) has shown that
very few symptoms are actually misdiagnosed as unexplained if
appropriate investigations have been carried out. Nevertheless,
where doubt exists, diagnoses should remain tentative until careful
follow-up has unequivocally ruled out a physical explanation
(Brown & Ron, 2002).
Treatment
Although a large proportion of unexplained symptoms remit
spontaneously, many continue to cause distress and disability over
time (e.g., Stone, Sharpe, Rothwell, & Warlow, 2003). Several
different treatment options are available, including short-term
group therapy (e.g., Kashner, Rost, Cohen, Anderson, & Smith,
1995), cognitive– behavioral therapy (CBT; e.g., Chalder, 2001)
and psychodynamic psychotherapy (e.g., Temple, 2001). Research
suggests that each of these treatments can be used successfully
with certain cases of somatoform illness (Blanchard & Scharff,
2002; Kashner et al., 1995; Kroenke & Swindle, 2000). Treating
these conditions can be notoriously difficult, however, and many
unexplained symptoms remain resistant to treatment. This is par-
ticularly true when symptoms are chronic or occur in the absence
of obvious psychopathology (Brown & Ron, 2002). In such cases,
somatoform illness is often managed by limiting patients’ expo-
sure to unnecessary investigations and interventions; encouraging
them (and their physicians) to accept a psychological interpretation
of their symptoms; and offering symptomatic treatments such as
pain management, physiotherapy, and occupational therapy (e.g.,
Brown & Ron, 2002; G. R. Smith, Rost, & Kashner, 1995). It is
noteworthy that the management approach in such cases is the
same regardless of the assumed etiology of the symptoms.
Theoretical Concepts
Recent attempts to explain the pathogenesis of medically unex-
plained symptoms can be grouped according to three explanatory
themes that are based on the concepts of dissociation, conversion,
and somatization.
 MECHANISMS OF MEDICALLY UNEXPLAINED SYMPTOMS
Dissociation
Probably the earliest systematic account of medically unex-
plained illness— originally couched in the language of hysteria—
was Janet’s dissociation theory (e.g., Janet, 1889, 1907; for theo-
retical origins, see Charcot, 1889). According to this account,
“hysterical” individuals experience a spontaneous narrowing of
attention when exposed to traumatic events. This narrowing of
attention leads to the development of unexplained symptoms via
two basic mechanisms. On the one hand, attentional narrowing
limits the number of sensory channels that can be attended to
simultaneously. Over time, the individual may develop a habitual
tendency to concentrate on some sensory channels at the expense
of others, leading to the loss of deliberate attentional control over
neglected channels. As a result, the individual is rendered anes-
thetic for any information in the previously unattended modality;
nevertheless, the information in this channel is still processed
outside conscious awareness (i.e., in a dissociated fashion). Janet
(1907) cited this mechanism as an account of unexplained sensory
loss, which at that time was regarded as a cardinal symptom of
hysteria.
Other symptoms reflect the activation of memories that have
become dissociated from the main body of knowledge representing
the patient’s personality. By this view, attentional narrowing cre-
ates a paucity of information within consciousness that prevents
new memories from being integrated with existing aspects of
personal knowledge. Because of the lack of competing informa-
tion, however, these memories may take on a compelling subjec-
tive quality that causes them to be misinterpreted as perceptions
rather than recollections. Moreover, in the absence of integration,
the patient has little or no control over the activation of these
memories, which may be triggered by related events in the internal
or external environment. According to Janet (1907), this process is
the same as that operating when comparable phenomena are cre-
ated using hypnotic suggestion. Indeed, Janet (1907) argued that
both suggestion and hypnosis are essentially pathological phenom-
ena, possible only in those individuals with the mental weakness
characteristic of hysteria.
Although a century old, the theoretical analysis offered by Janet
(1889, 1907) continues to influence nosology, theory, research,
and clinical practice concerning the somatoform and dissociative
disorders. Ludwig (1972), for example, argued that the primary
pathophysiological mechanism involved in the creation and main-
tenance of unexplained symptoms is an attentional dysfunction,
resulting from an increase in the corticofugal inhibition of afferent
stimulation (cf. Whitlock, 1967). This process of inhibition gen-
erates a dissociation between attention and sources of afferent
stimulation, preventing the integration of sensory information
within subjective awareness. In many respects, this view is a
modern-day manifestation of Janet’s (1907) argument that hyster-
ical phenomena arise from functional dissociations related to a
deficit in attention.
Evidence for afferent inhibition in unexplained illness was ob-
tained in an earlier electrophysiological study by Hernández-Peón,
Chávez-Ibarra, and Aguilar-Figueroa (1963). In that study, so-
matosensory evoked responses were found to be lower in the
affected leg of a patient with unexplained hemianesthesia when
compared with those evoked from the patient’s unaffected leg.
Other studies have failed to find this effect, however (Alajouanine,
795
Scherrer, Barbizet, Calvet, & Verley, 1958; Behrman & Levy,
1970; Halliday, 1968). Indeed, normal somatosensory evoked po-
tentials are often regarded as positive support for a diagnosis of
unexplained sensory loss. More recent electrophysiological studies
appear to suggest that conversion disorder is associated with
normal early evoked potentials but a disruption in the later P300
component (e.g., Fukudu et al., 1996; Lorenz, Kunze, & Bromm,
1998). These findings seem to indicate that conversion disorder
involves the selective attentional gating of processed information
at a late stage in the processing chain, prior to the generation of
conscious awareness (Sierra & Berrios, 1999). This is consistent
with Ludwig’s (1972) assertion that the inhibitory process in
unexplained illness occurs after cortical responses are evoked, at a
level beyond the primary receptor cortex.
Further evidence for Ludwig’s (1972) reinterpretation of the
dissociation model has been obtained in cognitive studies that
seem to confirm the presence of an attentional deficit in individ-
uals with unexplained illness. This deficit appears to extend across
a range of attentional measures, with patients showing decrements
on high-level tasks assessing vigilance, habituation, cognitive flex-
ibility, set shifting, and mental transformation (Bendefeldt, Miller,
& Ludwig, 1976; Hernández-Peón et al., 1963; Horvath, Friedman,
& Meares, 1980). Currently, however, the precise nature of this
attentional deficit remains unclear; further research using standard-
ized measures of attention, as well as controls for motivation and
anxiety, is required (Lader, 1982).
According to Janet (1889, 1907), the fragmentation of memory
associated with unexplained symptoms is triggered by the occur-
rence of traumatic events, which were regarded as having a desta-
bilizing influence on mental processing more generally. Consistent
with this, there is good evidence to suggest that traumatized
individuals have more dissociative experiences and more instances
of medically unexplained symptoms than those who have not
experienced trauma. Childhood sexual, physical, and emotional
abuse have all been linked to unexplained illness (e.g., Badura,
Reiter, Altmaier, Rhomberg, & Elas, 1997; Brown, Schrag, &
Trimble, in press; Kinzl, Traweger, & Biebl, 1995; Nijenhuis,
Spinhoven, van Dyck, van der Hart, & Vanderlinden, 1998; Pribor,
Yutzi, Dean, & Wetzel, 1993; Reilly, Baker, Rhodes, & Salmon,
1999; Roelofs, Keijsers, Hoogduin, Näring, & Moene, 2002;
Walker et al., 1988; for a review, see Brown, in press), and many
somatoform symptoms develop following exposure to acute stres-
sors (Binzer, Andersen, & Kullgren, 1997), such as recent loss
(Van Ommeren et al., 2001), relationship difficulties (Craig,
2001), and exposure to dead bodies (Labbate, Cardeña, Dimitreva,
Roy, & Engel, 1998). Nevertheless, a number of commentators
have questioned the necessity of identifying psychosocial precip-
itants in making a firm somatoform or dissociative diagnosis (e.g.,
American Psychiatric Association, 1994; Merskey, 1979; Ron,
1994; Wessely, 2001; cf. World Health Organization, 1992). Al-
though clear precipitants are often found, they are absent in many
cases (Ron, 1994; Wessely, 2001).
Although the similarities between Janet’s (1889, 1907) original
model and more recent accounts of medically unexplained symp-
toms (e.g., Kihlstrom, 1992; Ludwig, 1972; Whitlock, 1967) are
considerable, there is one fundamental difference. According to
Janet (1907), dissociation is an abnormal process provoked by
stress in the constitutionally weak mind of the hysterical patient; as
such, only those individuals with such a psychological weakness
796 BROWN
will experience dissociation and hence unexplained symptoms. In
contrast, the majority of contemporary models adopt the view that
dissociation is a normal psychological process, used by the organ-
ism as a defense mechanism in the face of trauma (see, e.g.,
Ludwig, 1972; Whitlock, 1967); unexplained symptoms arise
when this normally adaptive process is overgeneralized to a point
at which it becomes maladaptive. By this view, dissociation is a
coping response available to all individuals, although the degree to
which it is used varies from person to person.
Hilgard’s (1977) neodissociation theory, itself a partial rework-
ing of Janet’s (1889, 1907) original model, has been particularly
influential in its support of the notion that dissociation is an
adaptive mechanism that can become pathological if overused.
Unlike other models, Hilgard’s model is noteworthy in its assertion
that dissociation is actually a fundamental aspect of cognitive
processing in general, rather than an unusual response elicited by
traumatic events. According to Hilgard, the majority of behavior is
controlled by a set of functionally autonomous but interconnected
cognitive control systems (schemata) specialized for the execution
of particular behavioral acts. These control systems are hierarchi-
cally organized beneath an executive ego, which selects the cog-
nitive control systems required at any given moment. Once se-
lected, these systems are able to function without ongoing input
from the executive ego. This “dissociation” between the executive
ego and the systems responsible for action control allows well-
learned behaviors to be performed effortlessly, concurrently, and
outside awareness.
Although originally developed as a general account of the
mechanisms underlying behavioral control, neodissociation theory
has been particularly influential as an account of hypnotic behav-
ior. According to the theory, hypnosis represents one situation in
which the communication between individual control systems and
the executive ego is subject to change. Following suggestions
aimed at inhibiting the executive, a vertical dissociation can be
created within the ego forming two separate executive “streams,”
one of which is concealed beneath an amnesic barrier. This un-
conscious part of the executive is able to communicate with
targeted subsystems and therefore control behavior as normal,
although this is not represented in conscious awareness. As the
conscious part of the executive has no direct access to the systems
controlling the suggested behavior, it is perceived as occurring
involuntarily. More recently, Bowers (1992; see also Woody &
Bowers, 1994) has suggested that hypnotic phenomena result from
a horizontal dissociation between the executive and low-level
control systems. According to this “dissociated control” theory,
hypnosis serves to inhibit the executive altogether, allowing low-
level control systems to be automatically activated by the words of
the hypnotist. By this view, hypnotic involuntariness reflects the
fact that hypnotic phenomena are generated without executive
involvement (i.e., automatically).
Echoing the earlier work of Janet (1889), Kihlstrom (1992) has
applied neodissociation theory to the unexplained neurological
symptoms characteristic of the dissociative and conversion disor-
ders, citing the same kinds of functional dissociations as those
outlined by Hilgard (1977) for hypnotic phenomena. (For other
accounts that have endorsed the idea of common mechanisms for
hypnotic and unexplained medical phenomena, see Bryant & Mc-
Conkey, 1999; Ludwig, 1972; Oakley, 1999; Sackeim, Nordlie, &
Gur, 1979; Whitlock, 1967.) The symptoms of unexplained am-
nesia, for example, would be linked to a dissociation that prevents
the systems responsible for encoding and storing memorial infor-
mation from communicating with the executive (see Brown, 2002,
in press). Despite this lack of communication, memorial systems
themselves remain intact and continue to function as normal.
Compelling support for this hypothesis comes from an elegant
study by Kuyk, Spinhoven, and van Dyck (1999). Kuyk et al.
(1999) compared a group of patients reporting postictal amnesia
following nonepileptic seizures and a group reporting similar
memory loss following generalized epileptic events. All partici-
pants were hypnotized and given suggestions designed to facilitate
the recovery of material encoded during the ictal period. Using a
free-recall paradigm, 85% of the nonepileptic seizure patients
recalled events occurring during the ictus that could be corrobo-
rated by independent observations. None of the epilepsy patients
recalled ictal material. This study clearly demonstrates that the
nonepileptic attack patients had encoded information during the
ictal period but were unable to recall it because of a retrieval
deficit; in this sense, the “forgotten” material could be regarded as
dissociated from conscious awareness. The epilepsy patients, in
contrast, experienced a disruption in encoding during the seizure
and therefore had no ictal information in memory to retrieve.
Further support for this account comes from studies demonstrat-
ing that individuals experiencing unexplained blindness exhibit
intact visual perception in the absence of visual experience (e.g.,
Bryant & McConkey, 1989; Sackeim et al., 1979; for related
examples, see Kihlstrom, 1992; cf. Kirsch & Lynn, 1998). A
similar phenomenon is also observed in hypnosis, with participants
displaying intact processing of information that is otherwise un-
available to awareness because of suggestion (so-called implicit
processing; see, e.g., David, Brown, Pojoga, & David, 2000;
Kihlstrom, 1987, 1992). Other findings also lend support to the
notion that medically unexplained symptoms involve similar
mechanisms to those underlying hypnotic phenomena. Many un-
explained symptoms (e.g., amnesia, sensory loss, paralysis) have a
hypnotic counterpart, and these conditions are often accompanied
by high levels of hypnotic suggestibility (Bendefeldt et al., 1976;
Janet, 1907; Ludwig, 1972; Roelofs, Hoogduin, et al., 2002). There
is also good evidence to suggest that the occurrence of both
unexplained symptoms and suggested phenomena are subject to
similar moderating factors, such as belief, expectation, and atten-
tional focus (e.g., Kirsch, 1985; McConkey, 2001; Salkovskis,
1989; Tellegen & Atkinson, 1974). Furthermore, recent functional
neuroimaging studies provide some support for the idea that sug-
gested and unexplained medical phenomena involve similar cere-
bral mechanisms. In a positron emission tomography (PET) study
of unexplained paralysis, Marshall, Halligan, Fink, Wade, and
Frackowiak (1997) found increased activation in the right orbito-
frontal and anterior cingulate cortices, as well as an absence of
activity in the right primary motor cortex, when an attempt to
move the paralyzed left leg was made. A similar pattern of acti-
vation was found in a case of hypnotic left leg paralysis in a PET
study conducted by Halligan, Athwal, Oakley, and Frackowiak
(2000). These findings have been taken as evidence for the idea
that unexplained paralysis (both hypnotic and nonhypnotic) in-
volves the inhibition of primary motor activity by areas in the
prefrontal cortex (Halligan et al., 2000; Marshall et al., 1997).
Although its influence remains ubiquitous within contemporary
theorizing, a number of recent commentators have raised doubts
 MECHANISMS OF MEDICALLY UNEXPLAINED SYMPTOMS
about the explanatory significance of the dissociation construct
(e.g., Cardeña, 1994; Frankel, 1994). Frankel (1994), for example,
has argued that the concept of dissociation has been reified and
overextended within clinical practice to the point where it has only
descriptive and not mechanistic significance. According to
Frankel, any symptom that appears to involve some loss of control
or experience has been described by clinicians as dissociative,
despite there being no substantive grounds to assume that disso-
ciative mechanisms (in the Janetian sense) are responsible for the
clinical presentation in such cases (see also Brown, 2002; Cardeña,
1994). Depersonalization and derealization, for example, are typ-
ically regarded as dissociative phenomena (see, e.g., American
Psychiatric Association, 1994), despite the fact that neither in-
volves any profound alternation in perception, memory, or per-
sonal identity (World Health Organization, 1992). Indeed, recent
theoretical developments indicate that these phenomena involve
entirely different pathogenic mechanisms from those underlying
medically unexplained symptoms (Holmes et al., 2004; Sierra &
Berrios, 1998). This could explain why studies using measures
such as the Dissociative Experiences Scale (Bernstein & Putnam,
1986) have often failed to find elevated levels of dissociativity in
patients with unexplained symptoms (e.g., Alper et al., 1997;
Pribor et al., 1993; Roelofs, Keijsers, et al., 2002; for a review, see
Brown, in press). It is also possible to draw a meaningful link
between somatoform symptoms and hypnotic phenomena without
relying on the dissociation hypothesis (e.g., Oakley, 1999).
Conversion
The concept of conversion was introduced by Breuer and Freud
(1893–1895/1991) as an extension to Janet’s (1889, 1907) disso-
ciative framework. According to Breuer and Freud, the brain often
attempts to regulate the conscious experience of negative affect by
unconsciously suppressing (or repressing) the conscious recall of
memories associated with personal trauma. This process of repres-
sion can provide the basis for the creation of dissociated knowl-
edge structures that are kept outside awareness by an amnesic
barrier. Although the repression and dissociation of traumatic
memories may protect the individual from potentially overwhelm-
ing negative affect, this process prevents the neural energy asso-
ciated with that affect from being discharged in the usual fashion.
As this must occur if the energetic balance of the brain is to be
preserved, the negative affect is “converted” into a somatic symp-
tom that either was present at the time of the original trauma or is
some symbolic representation of it. In this way, the individual is
able to express psychological distress without consciously ac-
knowledging the psychic conflict responsible for it. As such,
unexplained symptoms can be viewed as serving a defensive
function, with the reduction of anxiety representing the primary
gain from developing symptoms; in contrast, any additional ad-
vantage associated with being ill (e.g., sympathy, attention, avoid-
ance of work) represents the secondary gain from symptoms. The
appeal of the conversion concept is well illustrated in clinical case
examples, such as that of the doctoral student who developed
right-arm paralysis shortly before the deadline for his dissertation.1
According to the conversion model, the student’s paralysis pro-
vides a means of avoiding his anxiety about completing, or failing
to complete, his dissertation in a way that is both emotionally
palatable and socially acceptable. Most clinicians with experience
797
of unexplained illness can describe cases of this nature, which
probably accounts for the continuing popularity of the conversion
concept within clinical circles.
This emphasis on the concept of psychological defense serves to
differentiate the work of Breuer and Freud (1893–1895/1991) from
the simple dissociation model described by Janet (1889, 1907).
According to this view, unexplained symptoms reflect an uncon-
scious emotional conflict that must be resolved if the patient is to
experience relief from symptoms. To achieve this, the underlying
conflict must be made conscious, and its accompanying affect
expressed appropriately (Temple, 2001). In earlier versions of the
theory (e.g., Breuer & Freud, 1893–1895/1991), the process of
conversion was viewed as the product of early sexual abuse. This
view was subsequently modified by Freud, who argued that pa-
tients’ memories of abuse actually reflect an unresolved Oedipus
complex driven by the repression of unacceptable sexual fantasies
concerning the opposite-sex parent (see Temple, 2001). In con-
trast, later analytic theorists have placed greater explanatory em-
phasis on patients’ internal representations of significant others
and their influence in subsequent relationships (e.g., Temple,
2001).
Although Breuer and Freud’s (1893–1895/1991) views concern-
ing psychic energies have long since been abandoned, the influ-
ence of these authors remains pervasive to this day. The notion that
hysterical phenomena are created by the conversion of psycholog-
ical distress into physical symptoms is widely endorsed, particu-
larly within medical circles. Like Janet’s (1889, 1907) model, such
a view is supported by studies showing that many patients with
unexplained illness have experienced extreme stress or trauma
(often sexual) prior to the development of symptoms (see Brown,
in press). In cases in which the patient reports no significant
psychological problems or early trauma, it is assumed that the
underlying conflict and its associated affect have been repressed
out of consciousness. The apparent lack of concern displayed by
many such patients, so-called la belle indifférence, is also regarded
as being consistent with the conversion concept (Iezzi & Adams,
1993). By this view, one would not anticipate significant psycho-
pathology in cases of unexplained illness if the patient were
successfully converting psychological distress into somatic
symptoms.
In addition, research concerning the alexithymia construct (Sif-
neos, 1973) has offered some support for the assertion that con-
version occurs as a means of discharging unexpressed emotion. A
number of studies have demonstrated that individuals who are less
able to identify and report on their emotional states (i.e., alexithy-
mia) are significantly more likely to exhibit unexplained medical
phenomena than those who do not display this tendency (e.g.,
Shipko, 1982). Other concepts introduced by Breuer and Freud
(1893–1895/1991) have been adopted by theorists working outside
a psychoanalytic framework. In particular, the concepts of primary
and secondary gain are consistent with a behavioral approach that
emphasizes the role of reinforcement in the creation and mainte-
nance of unexplained symptoms (Kellner, 1986). Some studies
suggest that clear gains are associated with many cases of unex-
plained illness (e.g., Raskin, Talbott, & Myerson, 1966).
1
I thank the anonymous reviewer who provided this case example.
798 BROWN

Despite its continuing popularity, there are significant problems

with the approach to unexplained illness described by Breuer and
Freud (1893–1895/1991). In particular, there are doubts surround-
ing the assumption that symptoms are necessarily the product of an
unresolved and unconscious psychological conflict (e.g., Ron,
1994; Wessely, 2001). Although obvious conflicts or psychosocial
precipitants are present in a proportion of cases, they are absent in
many others (for a review, see Brown, in press). According to the
psychoanalytic approach, such patients are unable to describe the
conflict underlying their symptoms because repression has ren-
dered it unconscious; the absence of apparent conflict is taken as
evidence for the operation of repression. Such circular reasoning
clearly raises doubts concerning the testability of the conversion
model. The problem is compounded by the assumption that unex-
plained symptoms are a symbol of the underlying conflict, rather
than a direct expression of it. Taken together, these assumptions
allow for an ad hoc approach to the formulation and treatment of
medically unexplained illness that may be both misleading and
potentially damaging. In particular, relentlessly probing for for-
gotten material, especially concerning sexual victimization, carries
a risk of creating compelling but false memories of abuse (see,
e.g., Lindsay & Read, 1994).
Research has also raised doubts concerning the validity of la
belle indifférence as a diagnostic indicator for the presence of
medically unexplained illness. Many patients with unexplained
symptoms are acutely upset about their problems (e.g., Lader &
Sartorius, 1968), for example, and an apparent indifference to
symptoms is also common in general medical illness (Brown, in
press; Gould, Miller, Goldberg, & Benson, 1986; Raskin et al.,
1966). Other studies have questioned the relationship between
alexithymia and unexplained illness (e.g., Cohen, Auld, &
Brooker, 1994), with evidence indicating that the measurement of
alexithymia is confounded by psychopathology in general (e.g., Figure 1. A multifactorial model of somatization. Reprinted from p. 353
of “Somatoform Disorders,” by L. J. Kirmayer and S. Taillefer. In S. M.
Bach, Bach, Böehmer, & Nutzinger, 1994). Research also suggests
Turner and M. Hersen (Eds.), Adult Psychopathology and Diagnosis, 3rd
that significant secondary gains are absent in many instances of ed., 1997, pp. 333–383. Copyright © 1997 by Wiley. This material is used
medically unexplained illness and are no more common than in by permission of John Wiley & Sons, Inc.
general medical illness (Brown, in press).

Somatization ease (i.e., symptoms), an attribution that may serve to generate

Dissociation and conversion represent the main conceptual pre-
cursors to contemporary accounts of unexplained illness based on
the concept of somatization. Lipowski (1968) has defined soma-
tization as the tendency to experience or express psychological
distress as the symptoms of physical illness. Somatization models
place less explanatory emphasis on the specific mechanisms of
unexplained illness, concentrating instead on the processes under-
lying normal somatic perception and the biopsychosocial context
surrounding the experience of physical and mental illness (for
reviews, see, e.g., Kellner, 1986, 1990; Kirmayer & Robbins,
1991a; Lipowski, 1988). Research inspired by the somatization
concept has identified a number of factors that may be important
in the generation and maintenance of medically unexplained symp-
toms. A recent model of the interaction between several of these
factors has been described by Kirmayer and Taillefer (1997; see
Figure 1). According to Kirmayer and Taillefer, illness, emotional
arousal, or everyday physiological processes produce bodily sen-
sations that capture attention to varying degrees. In some in-
stances, these sensations may be interpreted as indicators of dis-
illness worry, catastrophizing, and demoralization. As a result,
individuals may adopt the “sick role” by pursuing assessment and
treatment for their putative condition, thereby exposing themselves
to social forces (e.g., the reactions of others, the media, etc.) that
may reinforce their illness behavior and experience. Although such
a process is a normal response to the signs of illness, in some cases
it may reach disabling proportions, depending on the nature of the
individual and the sociocultural context in which he or she is
embedded. This process can be moderated by a number of con-
textual and dispositional factors, including previous illness expe-
rience; the response of significant others; illness worry; and indi-
vidual differences in personality, attentional set, coping behavior,
and autonomic reactivity (for evidence, see Kirmayer & Robbins,
1991a; Kirmayer & Taillefer, 1997; Robbins & Kirmayer, 1991;
the empirical literature in this area is discussed below).
The model provided by Kirmayer and Taillefer (1997) offers a
useful scheme for understanding the relationship between the
different factors underlying somatization. It is particularly appeal-
ing because it provides a model of normal illness behavior that can
be generalized to more maladaptive circumstances. The model also
 MECHANISMS OF MEDICALLY UNEXPLAINED SYMPTOMS
provides a useful account of the evolution of unexplained symp-
toms through its emphasis on the temporally extended aspects of
somatization. Moreover, it is consistent with the available empir-
ical evidence concerning the risk factors for medically unexplained
illness.
Despite its obvious appeal, however, there are a number of
problems with the somatization concept. In particular, it concen-
trates primarily on the factors that moderate the occurrence of
medically unexplained symptoms and only speaks in very general
terms about the psychological mechanisms involved in their me-
diation. Such a gap in the model is problematic because it obscures
potentially important etiological differences between different
types of somatization (Kirmayer & Robbins, 1991a, 1991b). Ac-
cording to Kirmayer and Robbins (1991a, 1991b), a distinction
should be drawn among unexplained physical symptoms that are
(a) the physiological components of anxiety or depressive psycho-
pathology ( presenting somatization), (b) normal bodily sensations
or minor pathological events that are misinterpreted as signs of
serious illness (hypochondriacal somatization), and (c) subjec-
tively compelling symptoms that cannot be attributed to either
physical or psychiatric illness or hypochondriasis (functional so-
matization). Although there is substantial comorbidity among
these different forms of somatization, they can be differentiated
both conceptually and empirically (Kirmayer & Robbins, 1991a,
1991b). Only the concept of functional somatization is of rele-
vance in this context.
Also problematic is the assumption that medically unexplained
symptoms are the result of identifiable physiological processes that
are exacerbated by social, cognitive, and perceptual factors. Al-
though this may be appropriate in some cases, particularly those
involving presenting and hypochondriacal somatization, it does not
provide a compelling account of the processes involved in the
generation of many medically unexplained complaints. It is, for
example, difficult to conceive of unidentified physical pathology
that could be responsible for the profound disruptions of function
observed in unexplained neurological illness.
A further problem is the assumption, intrinsic also to the con-
cepts of dissociation and conversion, that medically unexplained
symptoms must be the product of psychological distress. Although
such an assertion may be appropriate in the case of presenting and
hypochondriacal somatizers, this is not well established empiri-
cally in the case of individuals with somatoform (i.e., functional)
symptoms (Ron, 1994; Wessely, 2001).
Interim Summary
The dissociation, conversion, and somatization models have
added much to the field’s understanding of medically unexplained
illness. Each offers a different perspective on the pathogenesis of
these phenomena, and each is able to accommodate different
aspects of the available empirical evidence. The dissociation
model and its derivatives have helped illuminate the basic process-
ing mechanisms involved in the generation of unexplained symp-
toms. This perspective is supported by evidence from a number of
cognitive, electrophysiological, and neuroimaging studies. The
concept of conversion has extended the dissociation model by
providing a more detailed account of the way in which emotional
and motivational factors contribute to unexplained illness. The
conversion model is supported by research demonstrating that
799
traumatic events and other emotional disturbances are often asso-
ciated with the development of unexplained symptoms. More
recently, the somatization concept has placed current understand-
ing of unexplained illness in the wider biopsychosocial context,
providing a framework that elucidates the risk factors associated
with this phenomenon. Converging evidence from several different
sources supports this approach.
Nevertheless, it is clear that there are problems with the con-
cepts of dissociation, conversion, and somatization. Dissociation
models have been widely criticized for lacking precision (e.g.,
Frankel, 1994), something that has generated confusion about the
nature of dissociation as a psychological phenomenon. Although
concepts such as attentional gating and top-down inhibition have
advanced the argument, these are essentially descriptive labels for
the processes they purport to explain. In contrast, the conversion
model can be criticized for its circularity, something that has
rendered many aspects of this approach unfalsifiable. Moreover,
the fact that emotional and motivational factors appear to play a
significant role in only a proportion of cases of unexplained illness
casts doubts on the generality of the model (Ron, 1994; Wessely,
2001). The somatization approach can also be criticized for its
reliance on the concept of emotional precipitation, and its descrip-
tive nature prevents the generation of precise hypotheses.
An Integrative Conceptual Model of Medically
Unexplained Symptoms
The remainder of this article focuses on a novel account of
unexplained illness that builds on the strengths of existing models
while attempting to address some of their shortcomings. The
model is integrative in that it accommodates the basic elements of
the dissociation, conversion, and somatization concepts within a
common explanatory framework. As such, it should be viewed as
an extension of, rather than an alternative to, these approaches. The
model has two principal aims. First, it aims to provide a precise,
mechanistic account of how it is possible to experience compelling
symptoms in the absence of underlying pathology. Thus, the
proposed model explicitly assumes that genuine somatoform
symptoms are subjectively “real” (i.e., similar to explained phys-
ical symptoms) to the individual reporting them; the model there-
fore has little to say about malingering, which is regarded as a
separate phenomenon entirely. Second, the model aims to clarify
how the development and maintenance of unexplained symptoms
are moderated by different risk factors associated with the phe-
nomenon. In achieving these aims, the model attempts to explain
unexplained illness in a way that does not rely on the concept of
psychosocial precipitation but accommodates its undoubted im-
portance in many cases.
Explanatory Domain
The model is intended as an account of functional somatization
(Kirmayer & Robbins, 1991a, 1991b), encompassing all of the
DSM–IV somatoform and dissociative disorders, with the excep-
tion of hypochondriasis, body dysmorphic disorder, depersonal-
ization disorder, and dissociative identity disorder. Depersonaliza-
tion disorder is regarded here as distinct from other dissociative
phenomena, involving mechanisms that are qualitatively different
to those described below (Holmes et al., 2004). Dissociative iden-
800 BROWN
tity disorder, in contrast, may have certain mechanisms in common
with functional somatization, although a comprehensive under-
standing of this condition is beyond the scope of this model. Other
unexplained symptom syndromes, such as chronic fatigue, fibro-
myalgia, and irritable bowel syndrome, are also outside the remit
of this account, as are unexplained symptoms with an observable
physical component (e.g., phantom pregnancy). Finally, the model
does not attempt to explain why some individuals with unex-
plained symptoms display disproportionate levels of abnormal
illness behavior (Pilowsky, 1978; e.g., “doctor-shopping,” refusal
to comply with treatment, demands for repeated investigation).
Inevitably, there will be variation in the specific processes
underlying different medically unexplained symptoms. In line with
most previous theories in this domain, however, the model at-
tempts to provide a general account of medically unexplained
phenomena that can accommodate all members of this category.
Such an approach is necessitated by the fact that many individuals
suffering from unexplained illness are polysymptomatic, often
displaying a combination of neurological and nonneurological
symptoms. This approach is not without its critics. Kihlstrom
(1992), for example, has argued that the mechanisms of somato-
form complaints, including somatization disorder, are fundamen-
tally different from those involved in the generation of unex-
plained neurological symptoms (conversion disorder). However,
apart from differences in symptom numbers (including the pres-
ence of unexplained symptoms in other systems) and illness chro-
nicity, the available data indicate that there is very little that
distinguishes between conversion and somatization disorders
(Ron, 2001). Although such differences are important, they do not
provide sufficient grounds to assume a priori that fundamentally
different mechanisms are operating in these conditions.
It has also been argued that, unlike conversion disorder, soma-
tization disorder is simply an extreme form of abnormal illness
behavior, whereby symptom reports are used as a means of emo-
tional expression and social control (Kihlstrom & Canter Kihl-
strom, 1999). By this view, distortions in somatic perception (i.e.,
the experience of unexplained symptoms) may not be part of
somatization disorder at all. It is unclear, however, why the symp-
tom reports of patients with conversion disorder should be con-
sidered any more reliable than those of patients with multiple
unexplained symptoms. In the absence of data to the contrary, it
seems appropriate to pursue an explanation of unexplained illness
that can accommodate both neurological and nonneurological
symptoms.
Although the proposed model assumes that there are common
mechanisms underlying different unexplained symptoms, it is clear
that a range of factors moderate the occurrence of this phenome-
non and that the relative contribution of these factors will vary
from case to case. As such, exactly the same processes may not be
involved in the creation and maintenance of otherwise apparently
similar cases of unexplained illness. Moreover, if one regards the
development of medically unexplained symptoms as a temporally
extended process, it is possible that a variety of different moder-
ating factors will be implicated over the course of individual cases
also. In the next section, I describe the psychological character of
unexplained symptoms and the processes involved in their gener-
ation. The factors moderating the creation and maintenance of
these complaints are then addressed.
Attention, Consciousness, and Control
The central tenet of the proposed model is that unexplained
symptoms can be understood by reference to research and theory
from mainstream cognitive psychology. In particular, the model is
informed by research concerning the nature of different attentional
mechanisms in the cognitive system and their role in (a) shaping
the contents of consciousness and (b) controlling thought and
action.
At any given time, the cognitive system is inundated with
information that has the potential to influence thought and behav-
ior. The selection of relevant aspects of this information for further
processing and the control of action is generally regarded as one of
the most important tasks of the attentional system (Styles, 1997).
Much of the research in this area has focused on the so-called locus
of selection, that is, the point in the processing chain where
attentional selection occurs. Evidence suggests that complex per-
ceptual and semantic analyses are often performed prior to the
selection process (although see Lavie, 1995) through a parallel
spread of activation in associative networks triggered directly by
the receipt of sense data (e.g., Kosslyn, 1996; Marcel, 1983a,
1983b; Neely, 1977; Posner & Snyder, 1975; Rumelhart, McClel-
land, & the PDP Research Group, 1986; for reviews, see Styles,
1997, and Velmans, 2000). This spread of activation can be re-
garded as an inferential process (Sloman, 1996; Marcel, 1983a)
whereby existing knowledge assists in the identification of rele-
vant material for priority processing and hence attentional selec-
tion. The selection process itself is thought to integrate the most
active information in sensory, perceptual, and memorial systems,
producing multimodal representations that allow for the control of
routine behavior as well as further processing by attentional mech-
anisms at higher levels of the system (e.g., Allport, 1987; Colt-
heart, 1980; Crick & Koch, 1990; Logan, 1988; Marcel, 1983b;
Neuman, 1987; Norman & Shallice, 1986; Velmans, 1991, 2000);
the representations produced by this process are thought to relate
closely to the contents of conscious awareness (Allport, 1988;
Coltheart, 1980; Crick & Koch, 1990; Marcel, 1983a; Velmans,
1991, 2000).
A summary model of the cognitive system based on this re-
search is presented in Figure 2. In this model, the parallel spread
of activation in perceptual and memorial systems generates a
number of perceptual hypotheses, each representing a possible
interpretation of the stimulus world on the basis of previous
experience (Marcel, 1983a). The most active perceptual hypothesis
is then selected by a primary attentional system (PAS) and used to
organize relevant sensory information into integrated multimodal
perceptual units, or primary representations, that provide a work-
ing account of the environment for the control of action; in this
model, perceptual awareness corresponds broadly to the content of
these representations (cf. Allport, 1988; Coltheart, 1980; Crick &
Koch, 1990; Marcel, 1983b; Neuman, 1987). The PAS is influ-
enced by several factors, including the nature of the available sense
data, the activation of competing and complementary representa-
tions in memory, the selection threshold of the perceptual hypoth-
eses in question, and top-down input from high-level attention.
Behavior is controlled via two basic routes in this model, which
follows from the work of Norman and Shallice (1986). By this
view, routine behaviors are controlled by a hierarchical system of
procedural representations (schemata) specifying the attentional,
 MECHANISMS OF MEDICALLY UNEXPLAINED SYMPTOMS
Figure 2. The generation of experience and control of action by the cognitive system. Please note, the
activation levels of thought and action schemata are also influenced by the preattentive spread of activation in
the memory network (not shown).
cognitive, and motoric processes involved in executing well-
learned actions. In the proposed model, schemata are activated
automatically (in the sense used by Logan, 1988) by the construc-
tion of primary representations and are triggered when a threshold
level of activation has been reached (in accordance with a com-
petitive scheduling mechanism; see Norman & Shallice, 1986).
This automatic activation of schemata by the products of PAS
selection provides the system with a means of controlling cogni-
tion and action that is rapid, highly efficient, and consumes rela-
tively few processing resources. Behaviors controlled in this way
are experienced as occurring without conscious effort, whereas
perception and cognition at this level are associated with a sense of
intuition and self-evident validity. In situations in which the sys-
tem does not possess the appropriate schemata, an additional
means of control is required. In this model, novel actions are
controlled by a secondary attentional system (SAS; equivalent to
the supervisory attentional system in the Norman & Shallice, 1986,
model) that controls action indirectly by biasing the relative acti-
vation levels of schemata via the PAS, in accordance with general
purpose algorithms (for recent theoretical developments, see Bur-
gess & Shallice, 1996; Shallice, 1988; Shallice & Burgess, 1996).
The SAS is the province of self-regulatory processing, moderating
cognition and action in the pursuit of high-level system goals (cf.
Wells & Matthews, 1994). Processing controlled by the SAS
draws on a limited pool of resources, is perceived as mentally
demanding, and is associated with a sense of conscious volition
and self-awareness (cf. Norman & Shallice, 1986; Wells & Mat-
thews, 1994).
Medically Unexplained Symptoms as Alterations in
Perception and Control
The cognitive research and theory outlined above has a number
of important implications for understanding medically unexplained
801
illness. First, it suggests that the management of behavior is
governed by systems that operate without direct volitional control.
This is important in that it allows for functional dissociations
between the experience of volition and the control of thought and
action. Second, it identifies subjective awareness as a construction
or interpretation of the world rather than an unqualified account of
objective reality (for a similar view related to normal somatic
perception, see Leventhal, 1986). This underscores the fact that on
some occasions there may be no direct mapping between sensory
stimulation and the contents of subjective experience. Indeed,
there are numerous examples of how experience is often more
consistent with what people know, believe, and want to believe
about the world than with sensory data itself (e.g., hallucinations,
certain illusions, misperceptions, “perceptual set” phenomena, pla-
cebo effects, hypnotic phenomena, defense mechanisms; see, e.g.,
Bruner & Postman, 1949; Gregory, 1970; Hilgard, 1977; Vaillant,
1993; Wall, 1993). Phenomena of this sort are important because
they demonstrate how the generation of perceptual experience can
be overdetermined by prior information (e.g., memories) in the
cognitive system (Gregory, 1970; Leventhal, 1986). In the pro-
posed model, medically unexplained symptoms represent a com-
pelling example of this phenomenon.
By this view, unexplained symptoms arise when the chronic
activation of stored representations in memory causes the PAS to
select inappropriate information during attentional selection and
the automatic control of processing. The result is a misinterpreta-
tion of the sensory world that is experienced as subjectively valid
(i.e., “real” symptoms) because the individual does not have in-
trospective access to the inferences made during the creation of
experience and control of action. The nature of the resulting
symptom reflects the kind of information involved in this process.
Certain symptoms, such as those characterized by alterations in
experience (e.g., pain, feelings of discomfort, nausea, pseudohal-
802
lucinations), arise when inappropriate (i.e., inconsistent with in-
formation provided by the senses) perceptual hypotheses are se-
lected during the creation of primary representations by the PAS.
In contrast, symptoms characterized by an inability to control
perception, cognition, or action arise when inappropriate cognitive
schemata are automatically triggered by the process of PAS
selection.
In a case of unexplained sensory loss, for example, the relevant
schema would be one instructing the PAS to inhibit attention either
to a particular sensory modality (as in blindness or deafness), a part
of the body (as in focal sensory loss), or an aspect of the external
phenomenal world (as in tunnel vision). Similarly, dissociative
amnesia would be generated by schemata directing the PAS to
withdraw attention from certain types of memorial information or
inhibiting the operation of certain memory retrieval routines. Sche-
mata preventing the recall of all autobiographical information
would lead to amnesia with an associated loss of personal identity,
as observed in cases of dissociative fugue. In the case of certain
unexplained motor symptoms, schemata specifying particular limb
positions or body postures (as in fixed dystonia, gait disturbance,
etc.) or the inhibition of movement altogether (as in paralysis)
would be involved. In each case, this selection of inappropriate
schemata is often driven by the creation of relevant primary
representations by the PAS. In the case of unexplained paralysis,
for example, the underlying schema may be triggered by primary
representations consistent with the idea that limb movement is
deficient in some way.
Unlike other somatoform symptoms, unexplained seizures (so-
called nonepileptic attacks) are intermittent time-limited phenom-
ena that probably involve slightly different mechanisms to those
outlined above. Whereas other symptoms involve the chronic
activation and selection of perceptual or behavioral representa-
tions, unexplained seizures may involve the automatic activation
of a schema as an acute response to cues from the internal or
external environment (Brown, 2002). The same mechanism may
be responsible for other time-limited behavioral symptoms, such as
pseudoballismus (unexplained violent movements of the limbs,
akin to those seen in chorea). In cases involving repetitive move-
ments that occur in a time-limited fashion (e.g., tremors), schemata
may be subject to repeated reactivation through the operation of
the SAS. This notion accords well with the common clinical
experience that such movements are often considerably reduced
when the patient is distracted.
The model proposed here is clearly consistent with contempo-
rary dissociation theory, which asserts that unexplained symptoms
are generated preconsciously by an attentional gating mechanism
operating late in the processing chain (e.g., Ludwig, 1972; Sierra
& Berrios, 1999). It also captures Janet’s (1889) original idea that
unexplained symptoms reflect a distortion in awareness resulting
from information that has become “stuck” in the cognitive system
(so-called fixed ideas). The proposed model also assumes that a
horizontal dissociation between different levels of processing in
the cognitive system is central to all somatoform symptoms (cf.
Hilgard, 1977; Janet, 1907; Kihlstrom, 1992; Oakley, 1999). In-
deed, it is this assumption that allows the model to resolve the
apparent paradox presented by unexplained symptoms character-
ized by an inability to control perception, cognition, or action
despite repeated and honest attempts to exert control by the suf-
ferer. In this model, the experience of volition is associated with
BROWN
the operation of the SAS, but the ultimate locus of cognitive and
behavioral control is with the PAS and the schemata underlying
routine action. When the patient attempts to control cognition or
action, he or she is engaging the SAS; the attempt is unsuccessful
because the locus of the patient’s deficit is the chronic activation
and selection of representations by the PAS. One important impli-
cation of this approach is that symptoms are generated by psycho-
logical mechanisms but are not produced deliberately.
Unlike Janet’s (1889, 1907) original dissociation theory, how-
ever, the proposed model rejects the idea that unexplained symp-
toms are the product of a purely pathological process. In the
proposed account, symptoms result from a subtle disruption in
processes that are fundamental to the everyday control of behavior
and experience (cf. Hilgard, 1977; Kihlstrom, 1992); in this sense,
unexplained symptoms are essentially “normal” psychological
phenomena (cf. Halligan & David, 1999). This is clearly consistent
with epidemiological evidence demonstrating the ubiquity of un-
explained illness (Escobar et al., 1998; Fink et al., 1999; Kroenke
et al., 1997) and the fact that many individuals experience dis-
abling symptoms in the absence of other psychopathology (Wes-
sely, 2001).
The Origins of “Rogue Representations”
According to this approach, unexplained symptoms constitute
an alteration in the body image generated by information in the
cognitive system, rather than disturbances in the neural hardware
itself (cf. Leventhal, 1986; Ramachandran & Hirstein, 1998). The
term rogue representation is used here as a generic label for the
inappropriate information that is selected by the PAS during this
process. Broadly speaking, any kind of information within the
cognitive system concerning the nature of physical symptoms can
provide a template for the development of an unexplained com-
plaint. Rogue representations can therefore be acquired from many
different sources, including direct exposure to physical states in the
self, indirect exposure to physical states in others, the sociocultural
transmission of information about health and illness, and direct
verbal suggestion.
Exposure to physical states in the self. The fact that somato-
form patients often have a history of physical illness (e.g., Crimlisk
et al., 1998; Merskey & Buhrich, 1975; Slater & Glitherco, 1965;
cf. Schrag, Brown, & Trimble, 2004) suggests that many rogue
representations arise out of memory traces acquired during epi-
sodes of organic pathology. Similar traces are also established
when symptoms result from minor pathological events, such as the
loss of sensation in a limb following transient ischemia (Breuer &
Freud, 1893–1895/1991; see also Sharpe & Bass, 1992). The
physical components of emotional states, such as those associated
with anxiety (e.g., shaking, palpitations, nausea, muscle tension,
chest pain, dizziness, dysphagia, light-headedness, visual distur-
bance, tinnitus), also leave representations in memory that could
provide the basis for the later development of unexplained symp-
toms. Also included in this category are the sensorimotor compo-
nents of certain defensive reactions that can occur in response to
traumatic events, including numbing and analgesia (Nijenhuis,
Vanderlinden, & Spinhoven, 1998), freezing (Nijenhuis, Vander-
linden, & Spinhoven, 1998), the sham-death reflex, and the violent
motor reaction (Kretschmer, 1926; Ludwig, 1972). The storage of
representations pertaining to these events could account for some
 MECHANISMS OF MEDICALLY UNEXPLAINED SYMPTOMS
of the most common unexplained neurological symptoms, includ-
ing sensory loss, paralyses, and certain types of nonepileptic
seizure (Kretschmer, 1926; Ludwig, 1972; Nijenhuis, Vanderlin-
den, & Spinhoven, 1998). Arguably, traumatic experiences such as
physical or sexual abuse provide one of the richest sources of
material for the development of rogue representations, often en-
compassing organic damage, intense emotional arousal, and the
defensive use of physical reactions within the same experience.
Exposure to physical states in others. There is good evidence
to suggest that rogue representations can be acquired indirectly
through exposure to physical symptoms in others (e.g., Charcot,
1889; Fallik & Sigal, 1971; Van Ommeren et al., 2001). Many
somatoform patients have been exposed to abnormal levels of
illness in the family environment (Hotopf, Mayou, Wadsworth, &
Wessely, 1999), and unexplained complaints seem to be more
common in individuals who are exposed to physical illness on a
regular basis (e.g., medical students; Woods, Natterson, & Silver-
man, 1966). The effect is also illustrated by the occurrence of
so-called mass hysteria, when unexplained symptoms can spread
through a community like a contagious physical condition (e.g.,
Van Ommeren et al., 2001). To account for these findings, the
model assumes that observing symptoms in others creates memory
traces that are functionally similar to those generated when the
same symptoms are experienced in the self. This is consistent with
evidence demonstrating that observing actions in others creates
representations that are comparable with those involved in the
production of the same act (e.g., Jeannerod, 1994; Prinz, 1997;
Sebanz, Knoblich, & Prinz, 2003).
Sociocultural transmission. It is also well established that
unexplained symptoms can be shaped by sociocultural conceptions
of illness, with many somatoform phenomena conforming to a
popular conception of what constitutes a “genuine” symptom (e.g.,
Reynolds, 1869). Thus, a higher proportion of nonepileptic attacks
involve collapse or prominent motor activity when compared with
seizures resulting from epilepsy (Meierkord, Will, Fish, & Shor-
von, 1991). Similarly, the experience of nonpsychotic parasitosis
(the sensation of insects crawling beneath the skin) and burning
hands and/or feet, are considerably more common in African and
Asian cultures than in North America (American Psychiatric As-
sociation, 1994), demonstrating the role of local concerns about
illness in the development of unexplained symptoms (see Isaac et
al., 1995; Van Ommeren et al., 2001). Indeed, all cultures have
socially sanctioned models of illness (the so-called sick role;
Parsons, 1964) that are likely to shape the representations respon-
sible for the development of unexplained symptoms. These views
are generated and transmitted by many different sources, including
the family, the medical profession, the media, the Internet, and
society more generally (Fallik & Sigal, 1971; Stewart, 1990).
The proposed model assumes that the creation and alteration of
rogue representations through sociocultural transmission involve a
similar process to that operating when symptoms develop after
exposure to illness in others. In other words, exposure to general
information about physical illness creates memory representations
that are functionally equivalent to those encoded during episodes
of illness in the self. This is consistent with research showing that
executing an action and thinking about that action involve similar
neurocognitive processes (e.g., Jeannerod, 1994; Prinz, 1997). The
model also assumes that the activation levels of rogue representa-
tions are partly determined by the activation of any associated
803
representations in the memory network (Marcel, 1983a, 1983b;
Neely, 1977), including those representing conceptual and seman-
tic information. As a result, symptoms tend to become more
consistent with other information in the system over time (see also
Kihlstrom, 1992; Leventhal, 1986), which could help account for
the influence of beliefs in the development of unexplained
symptoms.
Verbal suggestion. The processes identified here as central to
the development of unexplained symptoms have also been linked
to the creation of hypnotic phenomena (Brown & Oakley, 2004; cf.
Janet, 1907; Kihlstrom, 1992; Ludwig, 1972; Bryant & McCon-
key, 1999; Oakley, 1999). Assuming that similar processes are
involved in these phenomena, it seems likely that some unex-
plained symptoms originate from rogue representations developed
in response to direct verbal suggestions, akin to those encountered
in the hypnotic setting. These could either be in the form of
autosuggestions (e.g., thinking “I still won’t be able to see when
they take the bandages off”) or heterosuggestions from relevant
others (e.g., being told “This may hurt” during a physical exami-
nation). This process may also overlap with that involved in
phenomena such as the placebo effect; in this case, however, the
result is the absence of genuine symptoms rather than the presence
of unexplained ones, reflecting the activation of different repre-
sentations in each case.
Self-Focused Attention and the Development of Symptom
Chronicity
According to this account, all people possess material about
symptoms that could provide the basis for rogue representations
and somatoform conditions. Although some people have much
more material in this respect, it is unlikely that this alone could
account for why there are such marked individual differences in
the tendency to develop unexplained symptoms. How does the
model account for these differences?
The answer to this question lies in understanding how the initial
selection of a rogue representation can lead to the development of
a chronic problem. Evidence from a number of sources suggests
that self-focused attention is an important factor in this respect.
Robbins and Kirmayer (1991), for instance, have identified a
body-focused attentional bias in patients with unexplained symp-
toms, and a link between self-focused attention and subjective
symptom reports has been obtained in several nonclinical studies
(e.g., Pennebaker & Brittingham, 1982; Wegner & Guiliano,
1980). A number of investigators, for example, have found that
introspective individuals are more likely to experience somatic
symptoms (e.g., Hansell & Mechanic, 1986; Pennebaker, 1982;
Robbins & Kirmayer, 1986), and manipulations aimed at directing
attention toward the self tend to increase physical symptom reports
(e.g., Pennebaker & Brittingham, 1982; Wegner & Guiliano,
1980). Evidence also suggests that elevated symptom reports are
associated with boring environments rather than stimulating ones,
apparently because of the decreased attentional load in the former
(e.g., Fillingim & Fine, 1986; Pennebaker & Lightner, 1980). In
addition, there is strong evidence that self-focus is a feature of
depression and anxiety (e.g., Hope & Heimberg, 1985; T. W.
Smith & Greenberg, 1981; Wells & Matthews, 1994), which often
occur alongside somatoform illness (Brown & Ron, 2002). Attend-
804 BROWN

ing to the body has also been identified as an important factor in

hypochondriacal somatization (Salkovskis & Warwick, 1986).
In the proposed model, the recurrent redirection of attention
onto symptoms by the SAS is the primary pathogenic factor in the
development of symptom chronicity (see Figure 3). Allocating
high-level attention to a symptom (e.g., checking to see if is still
present) serves to augment the activation of the rogue representa-
tion and lowers the amount of activation required for it to be
selected in future (i.e., the selection threshold). This is a relatively
self-perpetuating process, facilitated by the automatic allocation of
SAS-level attention onto environmental events that are consistent
with currently selected representations (a form of confirmatory
bias). If symptom-focused attention is maintained for a sufficient
period, the activation levels of rogue representations may become
high enough to ensure their continued selection over time. In such
cases, the generation of an unexplained symptom is complete.
According to this account, anything that serves to increase
symptom-focused attention will contribute to the development and
maintenance of medically unexplained symptoms. Included in this
category are the misattribution of symptoms to physical illness,
negative affect, illness worry and rumination, illness behavior, and
certain personality factors. To this extent, the proposed model
overlaps considerably with the model of somatization described by
Kirmayer and Taillefer (1997; see also Chalder, 2001). The rela-
tionship between these different factors is shown in Figure 4.
Misattribution of symptoms. It is well established that patients’
experiences of symptoms, and their behavioral responses to them,
are strongly influenced by how they interpret their symptomatol- Figure 4. Factors involved in the development of symptom chronicity
ogy (e.g., Cioffi, 1991; Leventhal, 1986; Pennebaker, 1982; Skel- (feedback loops to rogue representations not shown).
ton & Croyle, 1991). A number of studies have shown, for exam-
ple, that symptoms perceived as a sign of serious physical
pathology are more likely to attract attention than those that are system. On the one hand, misattribution may arise automatically
attributed to a benign cause (e.g., Cioffi, 1991). For this reason, it during the creation of primary representations by PAS selection.
is likely that misattributing somatoform symptoms to a serious Misinterpretations of this sort may be in the form of “negative
medical cause—akin to the catastrophic misinterpretation of nor- automatic thoughts” associated with a subjective sense of sponta-
mal sensations found in hypochondriacal somatization—will con- neity and inevitability (cf. Beck, 1976). On the other hand, mis-
tribute to their maintenance in many cases. interpretations may be the product of ruminative activity associ-
There are two basic routes to symptom misattribution in the ated with the SAS (see Illness worry and rumination section; also
proposed model, reflecting the hierarchical nature of the cognitive Wells & Matthews, 1994). In both cases, however, the product is
an escalation of negative affect and perceived disability, increased
worry and rumination about illness, and potentially inappropriate
illness behavior. In turn, these factors increase the likelihood of
symptoms being misattributed to a physical illness, setting up a
vicious cycle (see Figure 4).
It is likely that several different factors can contribute to the
misattribution of symptoms to a physical cause. Unusual, painful,
or debilitating symptoms are likely to be associated with a greater
degree of negative affect and are therefore more likely to be
appraised as a threat warranting attention and self-regulatory ac-
tion (Cioffi, 1991). Maladaptive beliefs concerning the nature of
health and the meaning of symptoms are also likely to be impor-
tant, particularly the beliefs that health is a state devoid of symp-
toms and that symptoms always indicate pathology, both of which
are commonly found in patients with unexplained symptoms (Rief,
Hiller, & Margraf, 1998). “Irrational” beliefs of this sort are likely
Figure 3. The role of secondary attention in the development of unex- to originate in the familial context, particularly where an individual
plained symptoms. Factors perpetuating the allocation of secondary atten- has been exposed to high levels of illness (Hotopf et al., 1999) or
tion to rogue representations are shown in the dotted box (see the Self- disproportionate parental concern over benign physical symptoms
Focused Attention and the Development of Symptom Chronicity section). (Benjamin & Eminson, 1992). In itself, catastrophic misinterpre-
 MECHANISMS OF MEDICALLY UNEXPLAINED SYMPTOMS
tation is not necessarily irrational, however. Indeed, attributing
subjectively compelling symptoms to a serious physical cause
could be regarded as a normal part of the sick role, particularly
where certain symptoms are concerned (e.g., unexplained neuro-
logical symptoms). It may even be positively sanctioned by contact
with health care professionals (Lipowski, 1988), who often collude
with patients’ attributions about their conditions (Salmon, Peters,
& Stanley, 1999), refer for unnecessary investigations and physical
treatments (paradoxically “to put the patient’s mind at rest”), and
even misdiagnose somatoform symptoms as physical problems
(Kouyanou, Pither, Rabe-Hesketh, & Wessely, 1998).
Negative emotional states. Negative affect is not only a prod-
uct of somatoform symptoms and their attribution to physical
illness but also a potential contributor to the development and
maintenance of these conditions. As well as increasing the likeli-
hood of catastrophic misinterpretation, ongoing negative emo-
tional states (such as those associated with anxiety and depression)
serve to increase symptom-focused attention (see Wells & Mat-
thews, 1994) and may trigger or perpetuate both rumination and
illness behavior. It is also possible that negative affect directly
influences the actual encoding and storage of rogue representa-
tions. Such a concept could help explain the spontaneous devel-
opment of unexplained symptoms in the face of acute stressors. It
may be that extreme fear or anxiety leads to the chronic selection
of rogue representations, rather like the acquisition of conditioned
aversion to noxious stimuli. A second, and perhaps related, pos-
sibility might be that symptoms are acquired as the result of a
spontaneous narrowing of attention occurring as a biological re-
sponse to extreme anxiety or fear (Cardeña & Spiegel, 1993; Janet,
1907). It may be that this narrowing of attention serves to increase
the activation level of rogue representations, thereby contributing
to the development of symptom chronicity.
Illness worry and rumination. Both negative affect and the
process of symptom misattribution trigger illness worry and rumi-
nation, which may play a particularly important role in the devel-
opment of symptom chronicity. Following Wells (2000), illness
worry and rumination are defined as repetitive forms of self-
regulatory activity by the SAS aimed at reducing the discrepancy
between current and desired states related to the presence of
physical symptoms. Subjectively, they are experienced as streams
of conscious, typically negative mental activity concerning the
nature, meaning, and implications of symptoms and appropriate
courses of action to be taken in their presence. They are also
associated with a state of self-focused attention and constant
monitoring of the body for symptom-relevant information. In
general, these forms of cognition contribute to the maintenance of
unexplained symptoms by perpetuating the allocation of high-level
attention to rogue representations (and other perceptual and me-
morial information that supports their activation) and by increasing
negative affect, symptom misinterpretation and illness behavior.
The degree of rumination and worry depends on a number of
factors, including the level of associated affect, the nature of any
symptom misinterpretation, and the information available to indi-
viduals about their problems. Certain beliefs may also perpetuate
illness worry and rumination, particularly “positive” metabeliefs,
which suggest that these processes are useful for ensuring appro-
priate vigilance, mental preparation, and illness behavior (Wells,
2000). By maintaining rumination and worry, however, such be-
liefs can have the paradoxical effect of perpetuating symptoms.
805
Once an individual has begun to worry and ruminate about their
symptoms, terminating these processes may prove difficult unless
symptoms improve. Over time, this may lead to the development
of a “cognitive–attentional syndrome” characterized by chronic
rumination, worry, and symptom focus; maladaptive coping; and a
reduction of central processing resources (Wells, 2000). This could
account for the attentional deficit seen in some patients with
unexplained symptoms (Bendefeldt et al., 1976; Horvath et al.,
1980; Janet, 1907). Chronic rumination may also lead to the
development of ruminative schemata that can be triggered by PAS
selection alone, producing the same cognitive effects in the ab-
sence of SAS-level activity (cf. Wells, 2000). In this way, a
previously held element of control over the processes involved in
the generation and maintenance of symptoms is lost.
Illness behavior. Depending on the way symptoms are inter-
preted, the individual may engage in several different types of
illness behavior, including “checking,” medical consulting, infor-
mation seeking, reassurance seeking, avoidance, and doctor shop-
ping, each of which directs attention toward the body and symp-
toms. Continued attempts to check whether symptoms are present
(e.g., by mentally and physically scanning the body) is likely to be
particularly important in this respect (cf. Salkovskis, 1989; Sal-
kovskis & Warwick, 1986), especially when behavior has become
automatized over time and introspective access to the process has
been reduced. Repeated help seeking may also be central in main-
taining attention to symptoms, especially when casual instructions
to keep an eye on symptoms explicitly endorse this process. In
addition, attempts to seek reassurance through the acquisition of
illness-related information (e.g., from the Internet) may serve to
increase anxiety and provides ambiguous material that could serve
as a basis for rumination, catastrophic misinterpretation, and the
development of new rogue representations. Similarly, doctor shop-
ping may lead to patients receiving conflicting advice and diag-
noses, increasing the likelihood of rumination and misinterpreta-
tion and reducing patients’ faith in the reliability of the health care
system. In contrast, avoidance of illness-related material serves to
prevent the disconfirmation of any negative beliefs about symp-
toms, as does avoidance of activities that are perceived as having
the potential to exacerbate symptoms (Chalder, 2001); the latter
may be particularly problematic in that it can lead to physical
deconditioning and health problems in its own right.
Personality factors. The proposed model is consistent with
evidence demonstrating that individuals with certain personality
features are particularly vulnerable to developing unexplained
symptoms. Trait measures of negative affectivity (Watson &
Clark, 1984), for example, consistently correlate with subjective
symptom reports but show little or no correlation with objective
health markers. Studies show that high negative affectivity is
associated with introspection, self-focus, worry, symptom misin-
terpretation, and illness behavior (Watson & Clark, 1984; Watson
& Pennebaker, 1989), each of which has been linked to the
development of unexplained symptom chronicity in this account.
In addition, individuals high in hypnotic susceptibility may be
particularly sensitive to the automatic activation of cognitive and
behavioral schemata by internal and external events (Brown &
Oakley, 2004), which could increase their vulnerability to devel-
oping somatoform symptoms.
806
Body-Focused Attention as Psychological Defense:
Conversion Reconsidered
The processes outlined thus far provide an explanation of how
unexplained symptoms can develop in the absence of trauma. Why
is a history of trauma so common in patients with these conditions?
The model accounts for this by assuming that traumatic events
such as physical, sexual, and emotional abuse often lead to the use
of body-focused attention as a means of avoiding the affect and
cognitive activity associated with experiences of this sort.
Under normal circumstances, the individual is able to manage
negative affect via self-regulatory processing and goal-oriented
action (Wells, 2000; Wells & Matthews, 1994). The high level of
negative affect associated with trauma, however, increases the
difficulty of effective self-regulation, particularly when previous
assumptions about the self, others, and the world have been vio-
lated by the nature of the traumatic event (cf. Horowitz, 1986;
Janoff-Bulman, 1992). Self-regulation may also be impeded by
appraisals indicating that externally oriented actions (e.g., resist-
ing, attempting to escape) could prove futile or even lead to
retaliatory revictimization. Under these circumstances, the system
is forced to rely almost exclusively on internal processes for the
regulation of traumatic affect. According to the proposed model,
one way of reducing this potentially overwhelming affect is to
divert SAS resources from self-regulatory processing and onto the
body. Such a strategy could be used both during an episode of
victimization and/or afterward, when a motivation to avoid
trauma-related material and its associated affect remains; this is
particularly likely in cases in which revictimization is perceived as
inevitable (e.g., in a consistently abusive family environment).
These defensive actions serve to protect the individual from over-
whelming affect, although the resulting body-focused attention
facilitates the creation and maintenance of unexplained symptoms
via the processes outlined above.
Peritraumatic body-focused attention would also increase the
salience of the physiological aspects of trauma-related emotion
(including those related to emotional behavior) while suppressing
its affective and cognitive components. This could go some way
toward explaining the development of symptoms that in the tradi-
tional conversion model would be regarded as symbolic of their
underlying psychodynamics. Thus, the rogue representation under-
lying a fixed dystonic hand could result from a clenched fist
associated with angry feelings experienced at the time of trauma;
the individual may not recall these feelings, however, due to the
inhibition of high-level cognitive and affective processing during
the event. Focusing attention on the body during trauma would
also augment the salience of other somatosensory or sensorimotor
experiences associated with the event, such as pain (cf. Badura et
al., 1997), sexual feelings and movements (cf. Betts & Boden,
1992), and different physical defense mechanisms (Nijenhuis,
Spinhoven, et al., 1998; Nijenhuis, Vanderlinden, & Spinhoven,
1998), which could lead to the development of symptoms that
recapitulate other aspects of the initial trauma. Where other effec-
tive self-regulatory strategies are unavailable, focusing attention
on the body may become a habitual mode of dealing with negative
affect and stressful life events, producing a traitlike vulnerability to
unexplained symptoms such as that seen in somatization disorder.
The development of symptoms also provides a way of express-
ing negative affect without acknowledging its psychosocial source,
BROWN
a concept that is central to the original conversion model. In
addition to the primary gain of reducing negative affect, symptoms
may also confer additional advantages to the individual, or sec-
ondary gains, with both positive (e.g., greater emotional support
and affection from others) and negative reinforcement (e.g., pre-
vention of revictimization) contributing to their maintenance (e.g.,
Breuer & Freud, 1893–1895/1991; Kellner, 1986; Kretschmer,
1926; Ludwig, 1972).
Implications
Treatment
The proposed model has obvious implications for the treatment
of patients with medically unexplained symptoms. Given the cog-
nitive foundations of the model, it is particularly amenable to CBT,
although other treatments such as psychodynamic psychotherapy,
physiotherapy, occupational therapy, and pharmacotherapy (e.g.,
antidepressants) are also consistent with this approach. Once the
extent of any physical pathology has been established and an
organic explanation for symptoms has been ruled out, the treat-
ment of choice depends on a detailed assessment of the patient’s
symptoms and the factors associated with their onset and mainte-
nance, including the number, nature, and history of both current
and previous symptoms; the presence of any obvious emotional or
relational difficulties associated with the onset of symptoms; the
nature and extent of emotional disturbance more generally; the
degree of disability associated with symptoms; the patient’s illness
beliefs and attributions about the causes of his or her symptoms
(particularly when anxious) and the patient’s tendency for cata-
strophic misinterpretation; the extent of any worry and rumination
about symptoms; the nature and extent of any illness behavior,
including body checking, help seeking and consulting behavior,
reassurance seeking, information seeking, avoidance, and doctor
shopping; any history of traumatic events, particularly in child-
hood; the presence of possible secondary gains (e.g., litigation
claims); and relevant personality factors (e.g., negative affectivity,
dispositional self-focus). The likely impact of these factors on the
individual’s tendency to allocate attention to symptoms should be
considered throughout. Establishing the possible origins of the
rogue representations underlying symptoms is not essential, al-
though doing so could assist in socializing the patient to a psy-
chological account of his or her problems.
The assessment provides the basis for an idiosyncratic formu-
lation identifying the factors involved in the creation of symptoms
and the processes maintaining symptom-focused attention, allow-
ing avenues for intervention to be identified. When symptoms are
thought to result from interpersonal difficulties and/or unresolved
emotional conflicts, such as those pertaining to early abuse or other
childhood traumas, psychodynamically oriented therapy may be an
appropriate treatment option. In cases in which interpersonal or
emotional conflicts do not appear to be relevant, or a psychody-
namic approach is precluded for other reasons (e.g., client prefer-
ence, unsuitability), the use of CBT is indicated. The present
model extends current cognitive– behavioral work in this area by
(a) providing a detailed rationale for the use of CBT with unex-
plained symptoms, (b) identifying the mechanisms involved in
clinical change, and (c) suggesting certain additions to the thera-
peutic arsenal.
 MECHANISMS OF MEDICALLY UNEXPLAINED SYMPTOMS
From the outset, efforts should be directed toward helping
patients accept a psychological interpretation of their problems.
This could be facilitated by presenting a rationale for therapy
based on the model proposed here. The advantage of this approach
is that it provides a normalizing interpretation of somatoform
illness that does not rely on the concept of unconscious conflict, an
idea that is often explicitly rejected by patients. Possible social-
ization exercises might include the use of analogies demonstrating
how experience often misrepresents reality, such as the placebo
effect, battlefield analgesia, and hypnotic phenomena. The creation
or removal of symptoms using suggestion or hypnosis may provide
particularly compelling real-time examples of this process (Oak-
ley, 2001). Once patients are suitably socialized to the model,
interventions aimed at reducing symptom-focused attention can be
considered. Maladaptive beliefs, catastrophic misinterpretations,
and illness behaviors can all be addressed using conventional
verbal and behavioral reattribution techniques, and the use of
controlled worry periods and “detached mindfulness” may assist in
minimizing patients’ worry and rumination about symptoms
(Wells, 1997, 2000). Symptom-focused attention could also be
addressed more directly by the use of techniques such as attention
training (Wells, 1990), which aims to foster increased control over
attentional processing. Unlike traditional CBT, the current ap-
proach also provides a rationale for the use of techniques such as
suggestion (with or without hypnosis), to deactivate rogue repre-
sentations more directly (Oakley, 2001), as well as treatments that
could help replace them with more adaptive representations (e.g.,
occupational therapy, physiotherapy). Finally, the role of possible
secondary gains should be considered and interventions applied
where feasible.
Testing the Model
At the heart of the present approach is the assumption that all
somatoform conditions (with the exception of those involving
observable physical phenomena) are governed by the same basic
mechanism, namely, the repetitive reallocation of high-level atten-
tion onto symptoms. This basic assumption allows for the gener-
ation of several novel hypotheses by which the model might be
falsified.
Hypothesis 1: The severity and duration of unexplained symp-
toms will be increased or decreased by manipulations directing
attention toward or away from symptoms, respectively. In addi-
tion to simple laboratory studies, this prediction could be assessed
clinically by investigating the impact of attention training (Wells,
1990, 2000), a procedure designed to improve attentional control
and the ability to focus externally, on patients with unexplained
symptoms.
Hypotheses 2a and 2b: Patients with unexplained symptoms will
show a symptom-focused attentional bias when compared with
nonsomatoform controls; individuals with a traitlike tendency to
develop unexplained symptoms will show a body-focused bias even
when asymptomatic. These hypotheses may be particularly ame-
nable to investigation using electrophysiological (e.g., event-
related potentials), neuroimaging (e.g., functional magnetic reso-
nance imaging) and cognitive (e.g., modified emotional Stroop)
paradigms.
Hypothesis 3: Individuals with a tendency to focus attention on
the body will be disproportionately vulnerable to developing un-
807
explained symptoms. This prediction could be addressed in stud-
ies investigating the comorbidity between unexplained illness and
other conditions associated with body-focused attention, such as
body dysmorphic disorder (e.g., Veale, 2001) and the eating dis-
orders (e.g., Fairburn, Shafran, & Cooper, 1999; for preliminary
data, see Krishnamoorthy, Brown, & Trimble, 2001). Further
research investigating the occurrence of unexplained symptoms in
individuals with personality traits such as high private self-
consciousness (Fenigstein, Scheier, & Buss, 1975) is also
warranted.
Hypothesis 4: The relationship between traumatic experience
and unexplained symptoms is mediated by the use of body-focused
attention as a coping strategy. The use of mediator analysis (e.g.,
Baron & Kenny, 1986) may be particularly useful in this context.
Hypothesis 5: Modalities affected by unexplained symptoms will
be associated with deficits in high-level postattentive processing
but not low-level preattentive processing. A number of different
cognitive methodologies could be used to assess this hypothesis
(see, e.g., Roelofs et al., 2001; Roelofs, van Galen, Eling, Keijsers,
& Hoogduin, 2003).
Hypothesis 6: The catastrophic misinterpretation of symptoms,
illness worry and rumination, illness behavior, and negative affect
are all linked to the occurrence and severity of unexplained
symptoms by their effect on symptom-focused attention and vice
versa. Multivariate research using appropriate analytic tech-
niques (e.g., mediator analysis, path analysis, structural equation
modeling) may be a useful option in this case. Such research could
also help identify which, if any, of these factors (or combination of
factors) is the most important in the development of unexplained
symptoms.
Further research should also be conducted to establish the va-
lidity of the link between suggestion and unexplained illness. In
particular, research should address the possibility of using sug-
gested phenomena as laboratory analogues of medically unex-
plained symptoms. The development of such analogues would
facilitate controlled investigation of the factors that mediate and
moderate the creation and maintenance of unexplained symptoms.
Other studies should further investigate the relationship between
unexplained illness and suggestibility, using well-defined patient
groups and validated instruments that assess both objective and
subjective responses to suggestions. It would also be instructive to
address levels of suggestibility in both hypnotic and nonhypnotic
contexts, with a view to assessing the relative contribution of
hypnosis and suggestibility per se to the creation of unexplained
symptoms (cf. Brown & Oakley, 2004; Kirsch, 1997).
Summary
This review has attempted to describe current theoretical models
of medically unexplained symptoms and the research cited in their
support. It is clear that research motivated by the concepts of
dissociation, conversion, and somatization has added much to the
understanding of unexplained symptoms. Nevertheless, it is clear
that there are certain shortcomings— both empirical and concep-
tual—with existing approaches in this area. In particular, none of
the available models is able to provide an adequate account of how
subjectively compelling symptoms can persist in the absence of
organic pathology. In this article, an integrative conceptual frame-
work that attempts to address these shortcomings, and that explic-
808 BROWN
itly endorses the idea that unexplained symptoms are subjectively
real to the sufferer, has been described.
The proposed model is consistent with Janet’s (1889, 1907)
dissociation theory in its assertion that symptoms are caused by
stored information in the cognitive system that disrupts the inter-
action between conscious and preconscious aspects of information
processing. In line with conversion theory, the model suggests that
this process is often driven by a defensive reaction that operates to
reduce the individual’s exposure to traumatic affect. Like somati-
zation theory, the model identifies symptom-focused attention as
central to the creation and maintenance of unexplained symptoms,
and highlights the importance of catastrophic misinterpretation,
illness beliefs, rumination and worry, illness behavior, negative
affect, and personality features in this process. Although consistent
with the concepts of dissociation, conversion, and somatization,
the model extends existing theories in this area by reformulating
them within a common explanatory framework that is based on
cognitive psychological principles. In this way, the model attempts
to place the current understanding of unexplained symptoms
within the remit of everyday psychology, allowing for a more
normalizing interpretation of this phenomenon. It is hoped that the
model provides a useful scheme for organizing existing research
and theory in this area, as well as an impetus for further research
into unexplained symptoms and the development of more effective
strategies for their treatment.
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Accepted March 3, 2004 䡲

Call for Nominations

The Publications and Communications (P&C) Board has opened nominations for the
editorships of Clinician’s Research Digest, Emotion, JEP: Learning, Memory, and Cog-
nition, Professional Psychology: Research and Practice, and Psychology, Public Policy,
and Law for the years 2007–2012. Elizabeth M. Altmaier, PhD; Richard J. Davidson, PhD,
and Klaus R. Scherer, PhD; Thomas O. Nelson, PhD; Mary Beth Kenkel, PhD; and Jane
Goodman-Delahunty, PhD, respectively, are the incumbent editors.
Candidates should be members of APA and should be available to start receiving manu-
scripts in early 2006 to prepare for issues published in 2007. Please note that the P&C Board
encourages participation by members of underrepresented groups in the publication process
and would particularly welcome such nominees. Self-nominations also are encouraged.
Search chairs have been appointed as follows:

• Clinician’s Research Digest: William C. Howell, PhD

• Emotion: David C. Funder, PhD
• JEP: Learning, Memory, and Cognition: Linda P. Spear, PhD, and Peter Ornstein, PhD
• Professional Psychology: Susan H. McDaniel, PhD, and J. Gilbert Benedict, PhD
• Psychology, Public Policy, and Law: Mark Appelbaum, PhD, and Gary R. VandenBos,
PhD

Candidates should be nominated by accessing APA’s EditorQuest site on the Web. Using
your Web browser, go to http://editorquest.apa.org. On the Home menu on the left, find
Guests. Next, click on the link “Submit a Nomination,” enter your nominee’s information,
and click “Submit.”
Prepared statements of one page or less in support of a nominee can also be submitted by
e-mail to Karen Sellman, P&C Board Search Liaison, at ksellman@apa.org.
The deadline for accepting nominations is December 10, 2004, when reviews will begin.