Rjohnson paper psy745

JOHN JAY COLLEGE OF CRIMINAL JUSTICE
Somatization and
Somatoform Disorders
Conceptualization and Assessment
Rebecca Johnson
12/1/2011

S o m a t o f o r m D i s o r d e r s R . J o h n s o n P a g e | 1
Somatization Disorder is one of five somatoform disorders listed in the DSM-IV-TR,
along with Conversion Disorder, Hypochondria, Pain Disorder, and Body Dysmorphic Disorder.
These conditions are defined by physical symptoms that are not explained by physical disease or
bodily pathology; or whose severity is greatly in excess to what would be expected in any
present medical illness. Unlike malingering or factitious patients—who profess false symptoms
to gain benefit or out of desire to inhabit a sick role, respectively-- patients with somatoform
disorders do not consciously or intentionally feign symptoms. Symptoms are truly experienced,
and cause considerable distress and impairment. Medically Unexplained Symptoms (MUS) have
also been referred to in the literature as Functional Somatic Symptoms (FSS), drawing attention
to the fact that despite apparent lack of medical cause they function identically to any “real”
somatic symptom.
Somatization is commonplace: the presentation of FSS is nearly universal in across
cultures globally (Aragona, Monteduro, Colosimo, Maisano, & Geraci, 2008). Patients with
unexplained symptoms appear in medical offices very often, with studies giving esti mates that
as many of 52% of all doctor visits and 30% of all primary care visits are prompted by one or
more FSS (Kirmayer, Groleau, Looper, & Dominicé, 2004). Thus somatization in itself isn’t
unusual; it crosses the threshold into pathological somatoform illness based on the number and
persistence of symptoms, distress and impairment deriving from the symptoms, and overuse of
medical services once medical cause has been ruled out.
Although Somatization Disorder is the primary focus of this review, research studies
often collectively examine somatoform disorders1--especially when considering controversies of
1
Briefly, the othersomatoform disordersinclude Hypochondria (fear or conviction that one has a specific illness);
Pain Disorder (where patientspresent only pain symptoms); Conversion Disorder (presentation of pseudo-

classification and diagnosis—or FSS as a construct independent of any particular diagnosis.
DSM-IV criteria for Somatization Disorder (SD) proper include all of the following: 4 pain
symptoms related to different bodily locations or functions ; 2 gastrointestinal symptoms; 1
sexual or reproductive symptom; and 1 neurological symptom (such as numbness, weakness,
dizziness). The patient’s history of symptoms must begin before age 30, occur over several
years, and result in significant social, occupational or other impairment. They must also, of
course, not be better explained by medical illness or condition or by use of a substance.
Incidence and Prevalence
Because SD diagnosis requires such pervasive and longstanding symptomology, it is one
of the least common somatic disorders. Lifetime prevalence of somatoform disorders overall is
about 1% , but the rate is only 0.4%-0.75% for SD (Ladwig, Marten-Mittag, Erazo, & Gündel,
2001) As many as 5x more women than men are affected by somatoform disorders (Karvonen et
al., 2004) with the gender difference for SD as high as 10 x greater for women2(Mai, 2004).
Somatization disorder is more common as well in persons of low economic or social status
(Cwikel, Zilber, Feinson, & Lerner, 2008).
The High Cost of Somatoform Disorders
Somatization disorder and FSS bring high personal and societal costs. Patients typically
spend years with painful and debilitating symptoms that defy explanation or effective treatment
and render them unable to effectively maintain employment, social interaction, or personal
relationships. One strong indication of the level of impairment is the fact that SD patients spend
neurological symptoms subsequent to a trauma or stressor); and Body Dysmorphic Disorder (pre-occupation with
perceived bodily defect or abnormality)
2
The gendergap in diagnosisis significantly smaller for Pain Disorder and Hypochondria than for Somatization
Disorder, Conversion Disorder , and Body Dysmorphic Disorder.(Ladwig, et al., 2001) (Kuwabara et al., 2007)

an average of 7 days of every month in bed (Bass, Peveler, & House, 2001). SD patients have
much higher suicide rates than other Axis I or Axis II disorders, prompting clinical advice to
screen for SD among depressed patients—or for suicidal ideation in SD patients—as it represents
a specific suicide risk. (Chioqueta & Stiles, 2004) Frustration is shared by doctors as well, who
spend a disproportionate percentage of time and effort treating SD patients, with little positive
effect. One line of research in recent years is devoted specifically to evaluating effective
strategies for physicians dealing with SD patients (García-Campayo, Claraco, Sanz-Carrillo,
Arévalo, & Monton, 2002).
SD and other somatoform disorders become societally important when considering the
marked overuse of medical services, and the associated medical and social costs. In an attempt
to explain symptoms and find relief, SD sufferers make frequent medical appointments, request
and receive myriad diagnostic tests, and undergo invasive and expensive treatments and even
surgeries, in the quest for relief. Studies find that SD patients tend to follow cycles of testing and
treatment that may be repeated and duplicated with multiple doctors over time (Crimlisk et al.,
2000). As a result SD patients use an estimated 9 times the level of medical services of non-SD
patients3 and one particularly telling finding revealed that somaticizers received more surgeries
over a 10 year period than patients with identified medical diagnoses. (Fink, 1992). In the United
States, this over-utilization of medical services translates to a financial cost of $256 billion a
year in the United States, due to incremental costs solely attributable to somatization (Barsky,
Orav, & Bates, 2005).
Conceptualization and Diagnosis
3
This is reduced to 2x when controlled for the costs of comorbid physical and psychological conditions

Somatoform illness is baffling, distressing, and costly; it therefore has attracted much
research attention over the past century. Professional discussions leading up to the publication of
the DSM-V have prompted controversy over the validity of the classification and
conceptualization of these disorders as a coherent group. The most basic concern is the
possibility for medical illness to be incorrectly diagnosed as somatization. As medical science
advances, there remains the ever-present possibility that medical causes heretofore unknown will
be discovered for some FSS, thus revealing a so-called mental disorder to be physical after all.
Even disregarding that possibility, the subjective criteria used for diagnosing somatization may
be problematic, as they typically require clinicians to define “excessive” symptoms and distress
in contrast to presumably normal levels. There are those who believe the current grouping of
somatoform disorders itself is flawed, bringing together disorders arbitrarily on the basis of
“bodily” symptoms, even though they may manifest differing etiology and presentation (Birket-
Smith & Mortensen, 2002; Noyes, Stuart, & Watson, 2008).
Various research studies have questioned the validity of the current diagnostic categories,
particularly in light of the fact that FSS may appear in many other disorders that are not
considered to be somatoform. For example, many mood disorders have somatic symptoms
specifically listed amongst their diagnostic criteria. Furthermore some somatoform disorders
may arguably better belong to another diagnostic category. For instance, many researchers
contend that Body Dysmorphic Disorder (BDD) ought to be considered a variant of obsessive
compulsive disorder, since its obsessional quality is more clinically salient than its focus on
bodily disfigurement (Merskey & Mai, 2005).
Some researchers also argue for a reclassification of FSS in general, with SD, Pain
Disorder, and Hypochondria listed as variants of a newly termed Health Anxiety Disorder. This

would be described by four criteria on a continuum, emphasizing the primary role of anxiety in
the disorders: 1) pre-occupation with the body, with heightened attention to bodily function and
sensation; 2) disease conviction ranging from slight suspicion to delusional belief in the presence
of disease; 3) fear of disease ranging from slight worry to obsessional anxiety; and 4) safety-
seeking or confirmatory behaviors ranging from simple self-checking and verbal reassurance-
seeking, to invasive and potentially iatrogenic procedures including surgery. (Creed, 2011).
Etiology
Many different theories about the causes and origins of somatization have been put forth
over the past century, beginning with Sigmund Freud’s classic conceptualization of “hysteria” as
the conversion of anxiety and repressed psychic distress into physical manifestations (Merskey &
Mai, 2005) . This led to hypotheses that psychological defenses such as repression and denial
cause somatization. While this belief was broadly held for much of the 20th Century it lacked
empirical support. Recently, a large, multi-country study of over 25,000 patients found no
association between physical symptoms and psychological symptoms, tending to invalidate this
etiological view (Simon, VonKorff, Piccinelli, Fullerton, & Ormel, 1999).
Research in the past 30 years has investigated other potential causal and risk factors for
somatoform illness. Those with the strongest research support include: inherited risk for
emotional responsivity to physical sensations; deficient emotional self-regulation; learned
behaviors and attitudes; and environmental factors.
Etiology: Inherited Risk for Emotional Response to Symptoms
The first category describes a set of inherited traits including somatic sensitivity, high
emotional reactivity to stimuli, and a predisposition to negative affect (studied operationally

often in terms of the personality trait of neuroticism). A study of 1688 mono- and di-zygotic
twins, and non-twin siblings, has found that inherited risk factors contribute about 30% to the
etiology of Somatization disorder (Kendler, Martin, Heath, & Eaves, 1995) According to this
perspective, somaticizing patients are thought to be especially sensitive to physical sensations,
and to swift intense and generally negative emotional reactions to, and interpretations of, these
sensations. Hammad, Barsky & Regestein (2001) studied both affective and CNS response in
SD patients vs. non-somaticizing controls, and found that SD patients have a lower threshold for
affective response to stimuli, and evince greater autonomic arousal in response, with slower
recovery to baseline and quicker re-arousal upon repeated exposure to stimulus. (Hammad,
Barsky, & Regestein, 2001). Barsky had earlier developed a theory of “somatosensory
amplification” by which a patient focuses on bodily sensations, perceives them as intense and
disturbing, and interprets them to be pathological. Continued attention to the symptoms, and
conformational bias against any information that refutes the patients’ suspicion of illness, creates
a feedback loop of emotional distress and autonomic arousal that amplifies anxiety and symptom
severity. (Barsky, 1992). The Hammad et. al. study (Hammad, et al., 2001) found that
hyperarousal was indeed positively correlated to somatization in participants, indicating that
somatically disordered patients were not only more easily aroused but also less likely to be able
to distinguish between physically threatening vs. non-threatening stimuli. This makes SD
patients less able to filter out irrelevant sensations, to habituate to them, and to inhibit reactive
central nervous system arousal.
High levels of arousal and emotional reactivity become translated into distress and health
anxiety when interpreted through the lens of negative affect. A tendency for negative affectivity
is thought to be an inherited, stable personality trait according to various personality theories,

and is encompassed by the personality factor of “neuroticism” described by the Five Factor
model of personality(Feldman, Cohen, Doyle, Skoner, & Gwaltney, 1999). Some research
indicates that a predisposition to negative affect is at least as influential an etiological factor for
SD, as somatic sensitivity. One study specifically compared the relative influence of each,
finding that in emotional reactivity is mediated by a negative bias in reporting style and not by
somatosensory amplification/symptom perception hypothesis. Thus negativity is more
responsible for FSS than either emotional reactivity itself or somatic sensitivity (Aronson,
Barrett, & Quigley, 2006).
Related to neuroticism/negative affect, alexithymia is a personality construct that seems
to increase the likelihood that symptoms will be misinterpreted. Alexithymia refers to difficulty
in identifying and describing one’s emotions, and such lack of self-understanding and clarity
may trigger or worsen negative emotionality in the face of unexplained physical sensations. De
Gucht and Heister (De Gucht & Heiser, 2003) found a moderate relationship between
alexithymia and somatization while ((Porcelli et al., 2003) found not only a strong association
between alexithymia and the presentation of functional gastrointestinal disorders, but also that
levels of alexithymia are predictive of treatment outcome. [details of studies needed here)
Etiology: Deficient Emotion Self-Regulation Skills
In concert with the inherited factors described above, a second set of factors are thought
to play a part in the development of somatoform disorders. These factors are related to
deficiencies in emotional self- regulation, and in patients’ in strategies for coping with
symptoms. Emotional self-regulation is a fundamental psychological skill that is usually learned
in early infancy, as a child develops self-soothing techniques to respond to physical sensations,
assuage emotional distress, and ensure his or her are needs met (e.g. crying to gain adult

attention; sucking the thumb, clutching a blanket)(Waller & Scheidt, 2006). Emotional regulation
skills are critical at all ages, as they allow individuals to interpret stimuli, evaluate which stimuli
warrant attention and/or emotional response, and calibrate that response to react in an
appropriate way. Failings in emotional self-regulation may have a causal role in FSS, as patients
fail to accurately interpret bodily sensations, give undue attention to non-threatening stimuli, and
become emotionally reactive as a result. Research suggests a cycle where patients with
somatoform disorders often are unable to accurately identify their emotions and sensations
(alexithymia), fail to self-soothe (emotional regulation) in response to their hyper-aroused state
(emotional reactivity); and rely on a limited, rigid and maladaptive set of coping strategies.
Ineffective coping strategies exacerbate their sense of lack of control, which increases anxiety
and negative affect, resulting in greater physical discomfort and emotional distress.
Although psychoanalytic theories of somatization have been generally set aside, there is
nonetheless evidence that use of defensive coping responses can contribute to the development
of somatoform disorders. Several studies have found a link between defensive coping strategies
and FSS, with Brosschot and Aarse describing a specific subset of SD sufferers: highly
defensive copers who show higher anxiety levels than do those using less defensive coping
mechanisms. Defensive coping, including avoidance and repressing behaviors, seems to be a by-
product of greater alexithymia and dissociation between affect and autonomic response, as well
as the cognitive attribution of symptoms more often to physical than to psychological causes.
(Brosschot & Aarsse, 2001).
Etiology: Learned Maladaptive Behaviors
The nature and severity of FSS are highly influenced by personal experience and societal
culture, and their presentation may be part of a repertoire of learned behaviors. Generally

speaking, every individual learns specific and unique meanings of illness, pain and
symptomology within his or her family. Thus some families encourage or embrace an broad
conception of illness, accepting and validating expression of many types of symptoms, including
relatively less severe pain, injuries and discomfort. Other families may discourage the expression
of illness and limit acceptance of only relatively very severe and/or painful symptoms. Families
and intimates also may learn to “communicate by symptom” with shared meanings allowing
symptoms to substitute for direct expression of feelings. For example, children may learn that
when their mother has a headache it means she’s unhappy. These learned attitudes influence the
interpretation and attentional focus paid to symptoms and may result in greater report of FSS in
families with inclusive conception of and high attention to illness. FSS may vary in type or form,
as well, depending on socio-cultural norms. Thus in North America, where heart disease is
prevalent and publicized, somaticizers more often present symptoms such as chest pain and
shortness of breath than do patients in countries where heart disease is less common (Kirmayer
& Young, 1998).
Researchers have found significant evidence that learned attitudes toward health, illness
and particular diseases and symptoms contribute to somatoform disorders. Craig & Boardman
1994 longitudinal study revealed that patients presenting FSS are significantly more likely to
have been sick or witnessed negative health events in childhood (T. K. Craig, Boardman, Mills,
& Daly-Jones, 1993). This exposure may have the effect of making illness seem a more likely
explanation for ambiguous somatic symptoms to FSS patients than to those without illness
experiences in childhood. In addition children and adults witness the secondary benefits gained
by ill members of the family, who may get extra attention, sympathy, and support. It has been

suggested that personal crisis may trigger somatization by triggering the need for extra care
during crisis (T. K. J. Craig, Drake, Mills, & Boardman, 1994).
Aside from witnessing or experience illness, other environmental factors serve to
heighten the risk of somatoform disorder, particularly parental neglect, non-contingent parenting,
and childhood trauma and abuse. With non-contingent parenting and neglect children receive
inconsistent and unpredictable responses to behavior and events in the home, causing confusion
that can contribute to alexithymia. Furthermore, effective emotional self-regulation-- learned via
stable child-parent interactions early in life—is impeded by childhood neglect and abuse, and
sexual abuse is particularly predictive of dissociative symptoms which may affect accurate
somatic perception and interpretation, both of which are implicated in somatoform illness
(Spitzer, Barnow, Gau, Freyberger, & Grabe, 2008). Post-traumatic stress reactions map closely
to the conditions that put individuals at risk for somatization: hyper-vigilance about physical
safety and bodily integrity, greater emotional reactivity, and negative interpretation of stimuli
(Spitzer et al., 2009). Post-traumatic response may be dissociative as well as overly reactive, so
that Conversion Disorder –characterized by dissociation—is more strongly linked to childhood
trauma than the other somatoform disorders as well. (Brown, Schrag, & Trimble, 2005)
State of the Research
Somatoform disorders are highly studied because of their enigmatic nature and high costs
to individuals and society. Prevalence rates are supported by large-scale and archival studies,
particularly in northern European nations with access to thousands of patients and patient records
in nationalized health care systems. For example one Danish team conducted a population based
survey of 7,466 people for somatization defined as having 6 or more symptoms in 2 or more
locations(Ladwig, et al., 2001). The findings from such a large, random sample pulled from the

general population should be statistically strong and robust. One limitation, however, derives
from self-reporting bias amongst respondents. Another study in Denmark attempted to correct
for this by using structured interviews to screen a stratified sample of 701 individuals culled
from 1785 consecutive patients in 28 medical practices. The patients were screened for mental
and somatic symptoms and substance abuse, and for a variety of particular psychological
diagnoses, resulting in findings that f 35.9% of the sample met criteria for somatoform disorders
(Toft et al., 2005). In this case, although self-report bias was minimized, the population studied
was not random but already self-identified as patients, which of course resulted in much higher
prevalence findings. Nonetheless prevalence findings seem to be supported by solid research
based on large samples from a variety of community and clinical populations (Cwikel, et al.,
2008; Karvonen, et al., 2004; Kato, Sullivan, & Pedersen, 2010; Ladwig, et al., 2001; Mai,
2004).
One of the most impressive studies – in terms of number of participants--screened over
28,000 twins via blind, computer-assisted, structured questionnaire for various types of FSS.
Confirmation of prevalence findings was incidental , to the main objective of this study, which
was to use latent analysis to discover the best way to categorize types of FSS, to in light of
controversies regarding the classification of somatoform disorders. The authors derived 5 factors
from their data, but their primary finding was that somaticizing patients seem to either present
with a single type of symptom or many diverse symptoms, demonstrating the need for two types
of diagnosis: simple vs. complex somatoform syndromes (Kato, et al., 2010). In addition to this,
the authors used comparative data from mono-zygotic and di-zygotic twins to estimate a 7%-
29% contribution of genetic influence in the development of various somatoform disorders. The
results of this study seem particularly robust given the great number of participants, the blind and

anonymous administration of the survey, and the use of structured questions to garner more
accurate responses. The fact that the respondents were twins allowed the authors to control for
genetic effects as well as ascertain the proportion of genetic influence in contributing to
somatoform disorders.
The Kato (2010) study’s attempt to deduce logical categories for the many types
of FSS, reflects growing advocacy for reassessment of somatoform disorders and possible
reclassification in the DSM-V. Several studies seek support for reclassification by looking at
overlap in symptomology of patients with different disorders. Typical of these studies is one
conducted by Espirito-Santos et al (2009) using twenty-six patients with conversion disorder, 38
with dissociative disorders, 40 with somatization disorder, and a comparison group of 46 patients
taken from a clinical setting. Participants answered questions (using relevant instruments) about
dissociation, somatoform dissociation, and psychopathological symptoms. SD patients and the
controls reported significantly fewer dissociative and somatoform symptoms than did the CD and
Dissociative Disorder patients. This suggests that Conversion Disorder is more closely related in
presentation and etiology to other Dissociative illnesses than to Somatization Disorder, and
should be re-classified accordingly (Espirito-Santo & Pio-Abreu, 2009). These studies are
suggestive but the findings are weakened by their small size, limited and non-controlled
population sampling, and the potential for self-report bias or errors, as well as by the fact that the
results reflect a single instance of testing.
Similar limitations apply to a number of studies that attempt to locate a biophysiological
basis or marker for somatization. These include MRI and SPECT studies of the brain, as well as
measurements of HPA and ANS response, with comparisons between SD and non-SD
participants (Atmaca, Sirlier, Yildirim, & Kayali, 2011; Hakala et al., 2004; Hakala, Vahlberg,

Niemi, & Karlsson, 2006). For example, Hakala, et al (2004) found bilateral enlargement of the
caudate nuclei—a part of the frontal “executive circuit” of the brain dealing with bodily
awareness-- in 10 female SD patients, as compared to 16 female healthy controls. This difference
in brain structure may be implicated in somatization. While these sorts of findings cannot be
faulted in terms of objectivity, they are limited in generalizability by small numbers, and the
interpretation of results requires knowledge about how the specific structures function to
influence somatization. They are useful studies for just this purpose—to suggest avenues for
future study to explain how biophysical processes contribute to somatoform disorders.
Advances in medical imaging and diagnostic technology has led to increased studies the
bio-physiological underpinnings of somatization (Ellenstein, Kranick, & Hallett, 2011). However
most investigators continue to focus on the opposite end of the theoretical spectrum, at the ways
somatization may be the result of environmental factors or learning. Such studies tend to
compare survey or interview data from SD vs. non-SD participants, seeking evidence of
associations between childhood history and somatization (Brown, et al., 2005) Craig, Boardman
et. al. however, undertook a longitudinal study of 45 London patients presenting with multiple
FSS, over 2 years (T. K. Craig, et al., 1993). The South London Somatization Study compared
45 patients with multiple FSS, to 48 matched non-somaticizing patients, and 118 healthy
participants, as to various childhood factors. Compared to non-somatic and healthy controls, the
somaticizing group was significantly more likely to have observed illness in a close friend or
family member during childhood, and more likely to have experienced parental neglect. A
second follow-up in 1994 further assessed whether, within the 38 weeks prior to symptom
emergence –participants experienced stressful events with secondary gain potential. As
hypothesized, significantly more FSS patients than controls had experienced such stressors, and

they were less likely than non-somaticizing controls to use neutralizing coping skills (as opposed
to defensive or other coping skills). This study suffers from the same problem of small sample
size as the earlier cited works, as well as the issues of self-report bias and potential coding error
of patient interviews by researchers. Nonetheless the results gain credibility from the fact that
they were derived from a controlled paired study, from multiple measurements taken over 2
years in order to confirm persistence and consistency of reported histories and changes in
presentation of symptoms.
Childhood experience of illness and early family attitudes are oft-cited precursors to
somatoform disorders, but they are not the only environmental influence. Childhood abuse and
trauma are also strongly associated with somatization. One study found that 54% of patients
with SD reported childhood sexual abuse, compared to 16% patients with mood disorders
(Morrison, 1989). To further understand the link between somatization and childhood abuse,
there have been various studies that compare the incidence and type of abuse reported by
participants with FSS to that reported by non-somaticizing controls (generally patients with
mood disorders such as Major Depressive Disorder). Typically, researchers attempt to increase
the rigor of interview-based studies by using a combination of structured interviews and self-
report, for participants drawn from clinical populations and matched for demographic factors if
possible (Brown, et al., 2005; Mai, 2004; Spitzer, et al., 2008). Using paired controls, Brown and
Schrag conducted precisely such a study with 22 SD patients and 19 medical comparison
patients, who were given structured clinical interviews to assess the childhood family
environment, and screen for several types of childhood trauma as well as dissociative symptoms
often found in somatic patients. The authors found that SD patients reported significantly greater
emotional abuse, more severe physical abuse, and more emotionally distant and unsupportive

family relations than the non-SD controls (Brown, et al., 2005). Chronic abuse was the most
predictive of SD in this study, while other studies have found childhood sexual abuse to be
particularly predictive of Conversion Disorder later in life (Spitzer, et al., 2008). While there
have been quite a few of these studies, and each has found some association between childhood
abuse and somatization, the precise nature of the association is unclear. Different types of abuse
have been implicated in different studies without consistent agreement except for the general
association to trauma. All do share similar limitations, in that they use small samples drawn from
clinical populations, using self-report and interview techniques that may admit bias and error on
the part of both interviewer and subject. Critics of the studies note that abuse in childhood often
coincides with confounding characteristics of home and childhood environment which could be
the source of risk for SD.
An extremely active area of research has to do with the influence of personality
characteristics such as affective negativity and alexithymia. Investigators generally seek to
discern the many complex interactions seemingly in effect between somatization and various
combinations of emotional reactivity, negative affect, and alexithymia and other potential
cognitive deficits. One of the only community-based studies was conducted by (Bailey & Henry,
2007) who sent surveys sent by mail to 565 randomly selected households in New South Wales,
with a response rate of 41% (n=301). The authors sought to explore the relative influence of
alexithymia and negative affectivity on somatization, using a novel alexithymia scale that
provides sub-measures of not only the cognitive aspects of alexithymia (identifying, describing
and analyzing emotions and sensations related to emotions), but also the affective aspects
(capacity for emotional arousal, and fantasizing). They hypothesized a stronger tendency to
somaticize among participants with both cognitive and affective alexithymia (“type I”) vs.

simply cognitive alexithymia with normal affective function (“type II”). In addition they
hypothesize that the effect of either type of alexithymia will be mediated by a tendency toward
negative affect. The survey instruments included three self-report scales including the
alexithymia scale described above, a scale for somatization, and one for depression and anxiety
symptoms. Survey submissions indicating type I or type II alexithymia, vs. no alexithymia, were
culled from the pool and further analyzed with regard to somatization and negative affect.
Results confirmed a stronger association between somatization and type I alexithymia, than
either type II or non-alexithymia. It also found perfect mediation of both identifying and fantasy
subscales of alexithymia by negative affectivity indicating that alexithymia alone does not
predict somatization but interacts with negative affectivity to produce FSS. The validity of the
results are bolstered by the fact that they were anonymously submitted by a fairly large
community-based sample whose demographic makeup was not significantly skewed from the
community as a whole. There are limitations of self-selection and self-report bias, particularly
since respondents were asked to report on recalled memory and observations which can be
notoriously inaccurate. This is all the more so with alexithymic individuals who by definition
may not be able to accurately recall and describe their cognitive and emotional states. However
the study is the first to tease out the differential effects of affective and cognitive aspects of
alexithymia and how these aspects are mediated by negative affectivity, helping to hone in the
precise interactions and providing directions for future investigation.
Future Research Needs
The research somatoform disorders and FSS presentation is quite extensive and has
advanced considerably in recent decades to include greater focus and more robust findings on the

bio-physiological basis for such disorders, as well as ever more nuanced understandings of the
complex interrelation of affective, cognitive, and autonomic function and response. This
represents an attempt to understand the essential nature of somatoform illness in order to better
guide assessment and treatment. Getting beyond the lay conception of symptoms as “all in the
mind” to a more exact understanding of precisely which cognitive, behavioral and physiological
traits underpin FSS, will allow clinicians to develop and implement more targeted and effective
treatment strategies. Such findings also may improve patient motivation for treatment, with
symptomology explained by concrete factors, in a less stigmatizing or blaming way. For this
reason it’s important to improve on existing studies by increasing the numbers and diversity (in
terms of community representation) of participants, and developing ways to overcome the
inherent bias and inaccuracy of many self-report scales and instruments.
In addition, there needs to be more research on how proposed cognitive and affective
deficits and personality styles interact with environmental factors-- such as family history of
illness, and childhood trauma—and with behavioral responses and coping strategies. All of these
combine to create the whole clinical picture, and treatment may need to address all factors to be
effective. Alternatively, research might indicate a need to prioritize treatment of specific factors,
for best effect, thus simplifying a potentially very complicated therapeutic process.
Family and environmental factors can also be more thoroughly investigated to discover
not only exactly which are most predictive of somatization, but also to identify potentially
protective rather than pathological factors. These can be analyzed, to help guide treatment by
promoting conditions that are protective and inhibitive against FSS.
Finally the debate over DSM-V classification of somatoform illness may have significant
impacts on the diagnosis and treatment of FSS and related syndromes. If different somatoform

disorders are re-assigned to other Axis I categories, diagnosis rates may change and treatment
may be conceptualized differently to align with treatments already in place for the new
categories. Researchers ought to investigate whether application of those treatments to newly-
inducted somatoform disorders is effective, and how treatment may need to be adjusted for these
specific presentations.
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