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Instructions:

Each speaker will prepare a syllabus that must be submitted through the online submission system.
The length of the syllabus will be no shorter than 4 single spaced pages in essay (not point) format, plus references.
Use single spaced, 11 point type and (if possible) Times New Roman font.
When typing the text use word wrap, not hard returns to determine your lines.
If headings and subheadings are used, these may be highlighted by using all caps and bold.
Do not use the header or footer feature or endnotes in preparing the text.
The submission must be submitted online.

Title:
SOMATOFORM DISORDERS

Learning Objectives:
1. recognize the signs, symptoms and history associated with the presentation and diagnosis of somatoform disorders;

2. differentiate neurological and non-neuroanatomical presentations;

3. discuss the diagnosis of somatoform disorders with patients and families to enable acceptance of treatment;

4. recognize the treatment options available for patients with somatoform disorders.

CME Questions:
1. The clinician should address which of the following issues in a person suspected of having a somatoform disorder:

2. The gold standard for diagnosing psychogenic nonepileptic seizures is:

3. Which of the following therapies has the least successful outcomes for patients with somatoform disorders:

Keywords (Max 5):


1. neuropsychiatry

2. somatoform disorders

3. conversion disorder

4.examination

5.treatment

Introduction/Abstract (Please see instructions for formatting details):


A century ago, neurology and psychiatry were practiced in a unified framework as neuropsychiatry. In the early 20th
century, divisions occurred in the fields and lines were drawn between those who evaluated and treated patients with
epilepsy, strokes, and migraines, and those with anxiety, depression, and schizophrenia. These divisions resulted in a
dichotomous view of the brain/mind and influenced how we assessed the two patient populations.

Every medical specialty has patients who overlap the boundaries of its practice. These patients require a broadened
perspective in their assessment. General neurologic training focuses its teachings on the elemental neurological exam,
and psychiatric training focuses on the mental status exam. Many times, one approach is used at the exclusion of the
other. How to best assess at bedside the borderlands of neurology and psychiatry (attention, alertness, cognition,
memory, motivation), truly can be a gray zone.
The future of neurology and psychiatry has been and will be largely influenced by two major areas of interface
neuroscience discovery in the past 20 years and during the decade of the brain, and by the practical needs of society as
felt in the growing elderly population. Neuroscience continues to yield greater advances in diagnosis and treatments for
brain/mind diseases. As the population ages, we will have to confront increasing needs for effective and safe
neurobehavioral management in patients with greatly prevalent neurodegenerative disorders.

In this session we review the literature on one of the most challenging and sometimes frustrating patient population, those
with somatoform symptoms. It is here, where medically unexplained symptoms present, that a combined neurologic-
psychiatric perspective is essential for diagnosis and management. To make the presentation both academically
informative and clinically applicable, an overview of each of the disorders in the somatoform disorders (SDs)
classifications is reviewed. The DSM-IV classifications included: Somatization Disorder, Undifferentiated Somatoform
Disorder, Conversion Disorder, Pain Disorder, Hypochondriasis, Body Dysmorphic Disorder, and Somatoform Disorder
Not Otherwise Specified. A comparison to the DSM-5 will be discussed [1, 2]. A number of these disorders are often
encountered in medical and neurological clinical settings. Examples of the examination in patients in the clinic with
somatoform disorders are given to aid in discerning distinguishing characteristics and semiology of the presentations.

Of equal importance is the discussion of patients who present with medically unexplained symptoms that diagnostically
are not a somatoform disorder in nature. Examples include Factitious disorder and Malingering.

Brief mention is also made of current diagnoses including chronic fatigue syndrome, fibromyalgia, chronic Lyme, and
multiple chemical sensitivities, which have elements of somatoform and other Axis I components.

The descriptive overview is followed by presenting diagnostic and treatment research in somatoform disorders that is
found in the literature and that we are conducting at Brown Medical School/Rhode Island Hospital.

The key points that will be discussed in the presentation are as follows:

1) There is a plethora of observational, phenomenological and diagnostic information on Somatoform disorders.


2) There is no serologic or imaging lab test that will definitively diagnose somatoform disorders. Nonepileptic seizures
(NES), however, are diagnosed with video EEG, the gold standard for NES diagnosis.
3) We have only a small but growing body of controlled data on somatoform disorders treatments.
4) Anxiety and depression occur commonly in patients with somatoform disorders.
5) Reviewing the extant literature on somatoform disorders treatment suggests that improved outcomes may be obtained
with intensive, multi-modal treatment of patients with somatoform disorders.

Body (Please see instructions for formatting details):


A Summary of Somatoform Disorders
[based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV)] [3]

Somatization Disorder
Diagnostic features
Multiple and recurring somatic complaints that begin before the age of 30 years and occur over several years, resulting in
medical treatment or impairment of important areas of functioning (i.e. socially, occupationally, etc.).

Undifferentiated Somatoform Disorder


Diagnostic features
Undifferentiated Somatoform Disorder is the category for somatoform presentations of one or more persistent physical
complaints that last for 6 months or more. These somatoform presentations do not meet the criteria for Somatization
Disorder, lacking the number of symptoms, the age of onset, and the timeline.

Conversion Disorder
Diagnostic features
Conversion symptoms are changes or deficits in voluntary motor or sensory functioning that are not are explained by
structural anatomical pathways or physiological mechanisms and are not intentionally produced. Motor symptoms or
deficits include impaired balance, coordination, gait, paralysis or paresis, aphonia, dysphagia, urinary symptoms or
seizures. Sensory symptoms include anesthesia or dysesthesia, diplopia, amaurosis, deafness and hallucinations.
Psychological factors are judged to be associated with the symptoms or deficits.

Pain Disorder
Diagnostic features
Key features of Pain Disorder are that the pain itself is grave enough to warrant clinical attention and is the primary focus
of the clinical presentation. Psychological factors are judged to play a significant role in the onset, severity, exacerbation,
or maintenance of the pain. Subtypes are described that best characterize the factors involved in the etiology and
maintenance of the pain. These include associated with psychological factors, associated with both psychological
factors and a general medical condition, and the final subtype, associated with a general medical condition, which is not
considered a mental disorder.

Hypochondriasis
Diagnostic features
Individuals with Hypochondriasis are preoccupied with unwarranted concerns of having a serious disease despite multiple
medical reassurances and a negative work up. The preoccupation is based on a misinterpretation of one or more bodily
sign or symptom, which could include bodily function, with minor physical abnormalities, or with vague and ambiguous
physical sensations.

Body Dysmorphic Disorder


Diagnostic features
Individuals with Body Dysmorphic Disorder are preoccupied with thoughts concerning imagined or slight defects in their
appearance. Such individuals may become extremely self-conscious and avoid work, school, and other public settings.
Areas of concern include hair thinning, acne, wrinkles, scars, vascular markings, pale or plethoric complexion, swelling,
facial asymmetry or disproportion, or hirsutism. Size or shape of other facial or bodily areas are also common
preoccupations. The thoughts may dominate their lives, spending hours a day thinking about their defect.

Somatoform Disorder Not Otherwise Specified


Diagnostic features
Somatoform Disorder Not Otherwise Specified is the category for somatoform symptoms that do not meet the diagnostic
criteria of any specific Somatoform Disorder. An example of a disorder in this category is Pseudocyesis, (i.e. a false
belief of being pregnant associated with objective signs of pregnancy, such as abdominal enlargement, reduced
menstrual flow, amenorrhea, subjective sensation of fetal movement, nausea, breast engorgement and secretions, and
labor pains at the expected date of delivery).

Factitious Disorder
Diagnostic features
An individual with Factitious Disorder is psychologically driven to assume a sick role, thus feigning psychological or
physical symptoms with no external motives. Symptoms or signs may be fabricated subjective complaints, self-inflicted
conditions, exaggeration or exacerbation of preexisting general medical conditions, or any combination of these. The
judgment that a particular symptom is intentionally produced is made both by direct evidence and by excluding other
causes of the symptom. An individual may deny taking medication for an illness even though blood tests state otherwise
(e.g. hematuria in a person with an elevated coag panel found to have anticoagulants in his possession). They may
present their history with dramatic flair, but with extreme vagueness and inconsistency. Some may engage in pathological
lying about the symptoms (i.e., pseudologica fantastica). Once recognized and confronted, inpatients with Factitious
Disorder, (also known as, Munchausens syndrome) may deny allegations or abruptly leave against medical advice.

Factitious Disorder Not Otherwise Specified (including by Proxy)


Diagnostic features
Disorders with factitious symptoms that do not classify as Factitious Disorder are categorized as Factitious Disorder Not
Otherwise Specified. An example of a Factitious Disorder Not Otherwise Specified is factitious disorder by proxy, when
an individual indirectly assumes a sick role by intentionally producing a feigned physical or psychological condition on
another person, such as a sibling or child, who is under that persons supervision. As with Factitious Disorder, there is no
external incentive involved.

Malingering
Diagnostic features
Malingering IS NOT a psychiatric condition but refers to the exaggeration or feigning of physical and psychological illness
to achieve personal motives, such as avoiding obligations at work, school, or the military. Individuals may also resort to
malingering to obtain drugs, financial compensation, win a law suit or avoid jail time.

Advances in somatoform diagnostic research

Diagnostic Measures
A common concern with diagnoses in the Diagnostic and Statistical Manual of Mental DisordersIV is that psychiatric
diagnoses have no physiologic correlates. While aggregate data on depression and anxiety states have revealed
alterations in the hypothalamic-adrenal-pituitary (HPA) axis, [4, 5] these findings are not applicable to the diagnosis of
individuals with major depressive disorders or post traumatic stress disorders. NES are the neuropsychiatric exception to
this rule, with diagnosis validated by a physiologic measure -- the gold standard, video EEG, which has excellent
interrater reliability [6], and with adjunctive differentiation from epilepsy using serum prolactin assay [7].

Neuroimaging studies in somatoform disorders


A study of 11 patients with NES and 12 healthy controls comparing resting state fMRI revealed stronger connectivity
values between areas involved in emotion (insula), executive control (inferior frontal gyrus and parietal cortex) and
movement (precentral sulcus) [8].

Structural neuroimaging (morphometric MRI) in 10 patients with conversion disorder compared to healthy controls
revealed smaller mean volumes of the left and right basal ganglia and smaller right thalamus in the conversion patients
[9]. Studies using SPECT and functional MRI have identified the anterior cingulate gyrus and the orbitofrontal cortex as
potentially mediating the hypothesized attention and inhibition findings seen in patients with sensory and motor
conversion disorders [10, 11]. Bilateral vibrotactile stimulation in three patients with sensory conversion disorders resulted
in activation of the contralateral primary somatosensory region (S1), but no contralateral activation was present during
unilateral stimulation of the affected limb [12].

Other case reports and small sample-size functional neuroimaging studies in patients with conversion disorders have
been appearing in the literature increasingly [13, 14], but it is premature to localize the conversion lesion. Sensory
gating may be affected in conversion disorders such as PMD [15]. Further studies of functional neuroimaging examining
striatothalamocortical circuits controlling sensorimotor function and attention may yield insights into the neural and
effective connectivity in NES and other somatoform disorders.

Management

Treatment of SDs involves a team approach and consists of correct diagnosis, presentation, acute and chronic
management. Along with diagnosing the presentation, identifying the associated comorbidities is important for treatment.
Most psychopathology underlying SDs is often due to one of two issues: psychosocial developmental environment or
prior trauma and abuse. In recent years, research has focused on psychopathology of the disorder, classification of the
diagnosis, and development of outcome measures. This focus on psychopathology has led to the development of
targeted treatment strategies that can be tested in hypothesis driven studies.

The treatment team involves the clinician to whom the patient presents (which is typically symptom matched to the
medical specialty for the organ, e.g. chest pain to the ER/cardiologist, or seizure to the ER/neurologist). Once the
appropriate tests have confirmed the absence of an anatomic/physiologic cause, a mental health professional
(psychiatrist/psychologist) is called in to rule out conversion. If the consult is not obtained in the inpatient setting, many
times, outpatient follow up does not occur. If the diagnosis is established and clearly conveyed to the patient and the
family, outpatient follow up can be established, where therapy can be initiated. The clinician to whom the patient
presented should continue to follow the patient as they are being treated by the mental health provider for continuity of
care and to mitigate unnecessary further testing.

Different types of treatment strategies have been used for management of SDs, including group therapy, family therapy,
cognitive behavioral therapy (CBT), antidepressants, and rehabilitation [16]. Behavioral modification has been used, as
opposed to utilizing a cognitive or psychodynamic approach, in some populations, with the hypothesis that psychogenic
neurological events are a reinforced behavior, especially in the intellectually deficient subpopulation. Recently, specific
treatments have been studied in systematic, controlled trials for the management of SDs [17]. One type of therapy that
has been used for various psychological and psychiatric disorders, including SDs, medically unexplained symptoms and
conversion disorders, is CBT [18]. CBT is a form of psychotherapy that can be administered as a time-limited treatment to
help a patient become aware of their dysfunctional thoughts and to maximize function by practicing new ways to think
about their symptoms and learning new ways to respond to them.

Conclusion
Patients with somatoform symptoms remain a conundrum in the neurologic and the psychiatric clinic. There may be a
number of interventions that may be effective, but in the absence of adequately powered phase III trials, we do not know
what the best treatment for somatoform disorders are [19]. The challenges in the difficult neuropsychiatric population with
somatoform disorders, many times having comorbid neurological and psychiatric disorders, were described in a study
examining methodology for NES treatment trials [20]. Building on data from smaller sampled studies[21], a multi-site
randomized controlled trial for NES revealed improvement in patients treated with an NES workbook [22]. The advances
made in NES from utilizing a multidisciplinary approach [23], and results from these trials will possibly have implications
for other somatoform disorders treatments.

CME Answers (Use lowercase letters if its an a/b/c option; feel free to include a description next to the correct
answer):
1. a. The patients understanding of the disorder, b. The presence of current psychiatric symptoms, c. The impact of the
symptoms on the patients life, work, and family, d. Past psychiatric history, e. All of the above. Correct Answer: E.

2. a. Serum prolactin, b. Routine EEG, c. History alone, d. Video EEG capturing a typical event. Correct Answer: D.

3. a. Group therapy, b. Cognitive behavioral therapy, c. Supportive therapy, d. Interpersonal therapy. Correct Answer: C.

References: (Author(s) Last Name separated by a Comma, Title/Article, Source (i.e. Journal Name), Volume #,
Page #, Year)
References

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2010;167(6):626-7.
2. Stone J, LaFrance WC, Jr., Brown R, Spiegel D, Levenson JL, Sharpe M. Conversion Disorder: Current problems
and potential solutions for DSM-5. J Psychosom Res. 2011;71(6):369-76.
3. TaskForceonDSM-IVTR. Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR. 4th, text revision ed.
Washington, DC: American Psychiatric Association; 2000.
4. Kunugi H, Ida I, Owashi T, Kimura M, Inoue Y, Nakagawa S, et al. Assessment of the Dexamethasone/CRH Test
as a State-Dependent Marker for Hypothalamic-Pituitary-Adrenal (HPA) Axis Abnormalities in Major Depressive Episode:
A Multicenter Study. Neuropsychopharmacology. 2005;epub:1-9.
5. Simeon D, Knutelska M, Yehuda R, Putnam F, Schmeidler J, Smith LM. Hypothalamic-pituitary-adrenal axis
function in dissociative disorders, post-traumatic stress disorder, and healthy volunteers. Biol Psychiatry. 2007;61(8):966-
73.
6. Syed TU, LaFrance WC, Jr., Kahriman ES, Hasan SN, Rajasekaran V, Gulati D, et al. Can semiology predict
psychogenic nonepileptic seizures? A prospective study. Ann Neurol. 2011;69(6):997-1004.
7. Chen DK, So YT, Fisher RS. Use of serum prolactin in diagnosing epileptic seizures: report of the Therapeutics
and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2005;65(5):668-75.
8. van der Kruijs SJ, Bodde NM, Vaessen MJ, Lazeron RH, Vonck K, Boon P, et al. Functional connectivity of
dissociation in patients with psychogenic non-epileptic seizures. J Neurol Neurosurg Psychiatry. 2011;83:239-47.
9. Atmaca M, Aydin A, Tezcan E, Poyraz AK, Kara B. Volumetric investigation of brain regions in patients with
conversion disorder. Prog Neuropsychopharmacol Biol Psychiatry. 2006;30(4):708-13.
10. Vuilleumier P, Chicherio C, Assal F, Schwartz S, Slosman D, Landis T. Functional neuroanatomical correlates of
hysterical sensorimotor loss. Brain. 2001;124(Pt 6):1077-90.
11. Mailis-Gagnon A, Giannoylis I, Downar J, Kwan CL, Mikulis DJ, Crawley AP, et al. Altered central somatosensory
processing in chronic pain patients with "hysterical" anesthesia. Neurology. 2003;60(9):1501-7.
12. Ghaffar O, Staines WR, Feinstein A. Unexplained neurologic symptoms: an fMRI study of sensory conversion
disorder. Neurology. 2006;67(11):2036-8.
13. Spence SA, Crimlisk HL, Cope H, Ron MA, Grasby PM. Discrete neurophysiological correlates in prefrontal
cortex during hysterical and feigned disorder of movement. Lancet. 2000;355(9211):1243-4.
14. Marshall JC, Halligan PW, Fink GR, Wade DT, Frackowiak RS. The functional anatomy of a hysterical paralysis.
Cognition. 1997;64(1):B1-8.
15. Voon V, Gallea C, Hattori N, Bruno M, Ekanayake V, Hallett M. The involuntary nature of conversion disorder.
Neurology. 2010;74(3):223-8.
16. Hopp JL, LaFrance WC, Jr. Cognitive behavioral therapy for psychogenic neurological disorders. Neurologist.
2012;18(6):364-72.
17. Kroenke K. Efficacy of treatment for somatoform disorders: a review of randomized controlled trials. Psychosom
Med. 2007;69(9):881-8.
18. Kroenke K, Swindle R. Cognitive-behavioral therapy for somatization and symptom syndromes: a critical review
of controlled clinical trials. Psychother Psychosom. 2000;69(4):205-15.
19. LaFrance WC, Jr. Treating patients with functional symptoms: One size does not fit all. J Psychosom Res.
2007;63(6):633-5.
20. LaFrance WC, Jr., Blum AS, Miller IW, Ryan CE, Keitner GI. Methodological issues in conducting treatment trials
for psychological nonepileptic seizures. J Neuropsychiatry Clin Neurosci. 2007;19(4):391-8.
21. LaFrance WC, Jr., Miller IW, Ryan CE, Blum AS, Solomon DA, Kelley JE, et al. Cognitive behavioral therapy for
psychogenic nonepileptic seizures. Epilepsy Behav. 2009;14(4):591-6.
22. LaFrance WC, Jr., Frank Webb A, Blum AS, Keitner GI, Barry JJ, Szaflarski JP. Abstract 1.218. Multi-center
Treatment Trial Pilot for Psychogenic Nonepileptic Seizures. Epilepsy Curr. 2013;13(supp 1):99.
23. Schachter SC, LaFrance Jr WC, editors. Gates and Rowan's Nonepileptic Seizures. 3rd ed. Cambridge; New
York: Cambridge University Press; 2010.

Portions of this syllabus were used for the publication:


LaFrance Jr WC, Somatoform disorders. Semin Neurol 2009;29(3):234-246.

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