Three Theoretical Framework of Dissociative or Somatoform Disorders

Written by Grace Lian-Bodenbach , DMin, MDiv. BA (Psych) and Dr. Raja Paulraj, MD , psychiatrist, and non-resident scholar of Duke University Medical Centre for Spirituality, Theology and Health.
Last updated May 20, 2021

What is Functional Neurological Symptom Disorder?

This a newer term for conversion disorder. The patient has symptoms that are physical but cannot be account for by medical nor neurological disease. The symptoms are dissociative in nature. Please see below for more details.

What are the symptoms of conversion disorder?

What is conversion disorder (also called Functional Neurological Symptom Disorder)?

According to the ICD-10 classification, conversion disorder falls under the category of dissociative disorders.  Conversion disorder (CD acronym will be used henceforth) involves the loss of or interference with movements or loss of sensations, (ICD-10) which can begin as early as adolescence.  Psychological factors are judged to be associated with the symptoms or deficits (ICD-10).  The symptoms are not intentionally produced and feigned as in Factitious Disorders or Malingering.  The patient, therefore, presents as having a physical disorder, although none can be found that would explain the symptoms.  The symptoms can often represent the patient’s concept of the physical disorder, which may be at variance with physiological principles.  The assessment of the patient’s mental state and social situation usually suggests that the disability results from the loss of functions from a stressful life situation or conflict. Although problems or conflicts may be evident to others, the patient often denies their presence and attributes any distress to the symptoms or the resulting disability (ICD-10).

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Can it be co-morbid with  anxiety or depression?

Currently, there is much variability in the prevalence rates between genders, countries, clinical and non-clinical settings. Prevalence is hard to discern as there are many studies, which yield significantly different prevalence rates.  Much of the variability comes from various studies that were conducted in different countries and illustrates that cultural factors greatly impact how a clinician understands and diagnoses conversion disorder.  The prevalence rate in clinical and non-clinical settings varies between 5%-20% (Feinstein, 2011).  According to Feinstein’s (2011) study conducted in a general hospital setting, an estimated 20% of patients have symptoms of conversion disorder, while 5% of patients meet the criteria for the full syndrome.

Furthermore, he argues that one in five outpatients seen in a neurology clinic may have symptoms that cannot be attributed to a neurological disease (Feinstein, 2011).  His research also challenges accepted norms for the demographics of individuals likely to suffer from conversion disorder.  The general consensus is that this disorder is more predominant in young men who are struggling to obtain their education or women from rural areas, the less educated, or those in low socio-economic situations (Deka, Chaudhury, Bora & Kalita, 2007).  This is in contrast to Freud (1953), who depicted women to have this disorder more than their male counterparts as he viewed women as dependent and hysterical.  Instead, Feinstein (2011) found prevalence rates vary depending on the patients’ demographics.  It seems that the male patients dealing with great stress may have a co-morbid diagnosis with depression, anxiety or post-traumatic stress disorder (PTSD).  Therefore, Feinstein (2011) concluded that patients may be any individual who had significantly stressful events occurring in their lives.

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Theoretical framework that is culturally sensitive:

The current research will illustrate the importance of the theoretical framework a clinician uses, and how it greatly impacts the prevalence  rates of conversion disorder.  As well, we will see that etiology also impacts a clinician’s ability to decipher co-morbidity with other diagnoses such as depression and anxiety.  Cultural considerations are needed in examining the etiology and conceptualization of this disorder with an appropriate theoretical framework.

A brief overview will be presented on three theoretical frameworks that have been used to understand conversion disorder.  These frameworks include Freud’s theory of somatoform disorder and immature defense mechanisms, Janet’s theory of dissociation and trauma and Bandura’s social modeling theory.  As well, cross-cultural research has presented an alternative conceptualization such as Bandura’s social modeling theory (Syed, Effendi & Mehmud, 2011).  Recent neurological studies have bolstered support for Janet’s argument for trauma and dissociation etiology (Heruti et. al, 2002; Kanaan, 2009).  For example, a patient may state that he has pain in his leg, so much so that he is immobilized and must stay at home, and consequently, he is unable to attend any family gatherings or go to work.  However, after medical exams were conducted, there was no medical explanation for his pain and disability.  A psychological interview and investigation later revealed that the patient had much strife with his family members and had no desire to work at the family’s farm.  However, this perspective is not known to the patient, who genuinely wants to work and has for many years worked with his family members.  The precipitating stress and conflict is that the family’s farm has recently been sold to one of his brothers, and there is much dispute over this decision.  Often, this diagnosis is seen to be correct, when treatment and improvement involves the modification or absence of the stress triggers. Therefore, in the case of this patient, when he is told that the family will alleviate him of his responsibilities on the farm and allow him stay at home, and contribute to the family in another way, it seems his symptoms of pain slowly disappears.  On-going therapy helps him gain insight to the stress triggers and he learns how to deal with this stress and conflict.

The criterion for conversion disorder is to explore unexplained symptoms or deficits affecting voluntary motor or sensory functions that suggest an absence of neurological or other general medical condition.  Psychological factors are judged to be associated with the symptoms or deficits.  Although the inclusion and exclusion factors are similar in the two most common diagnostic manuals, the difference between the ICD-10 and DSM V in regard to CD is in classification.

There are different theories about the cause of CD from conflicts resulting in immature defense mechanisms, stress-diathesis-trauma model, learned maladaptive behaviors to cultural beliefs, which will be discussed in greater detail in the subsequent section (Ruddy & House, 2009).

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Freud (1856-1939) and Janet (1859-1947) were the two leading psychologists of their era and held prominent perspectives on this disorder.  In the beginning of his career, Freud considered hysteria (now renamed conversion disorder) to be a trauma-based disorder (Sar, Akyuz, Kundakci, Kiziltan &Dogan, 2004).  However, Freud later conceptualized the somatoform symptoms of hysteria as the result of a neurotic defense mechanism and referred to them as conversion disorder symptoms (Schwartz, 2011; Sethi &Lal, 2009).  The Freudian perspective of CD views the patients’ repression of their psychological distress into a somatic dysfunction, which is believed to be a defense mechanism of hysterical personalities (Shalev &Munitz, 1986).  Freud provided an understanding from a psychodynamic background and etiology of conversion disorder.  According to Freud, the patient has an impulse or wish that cannot be fulfilled due to negative connotations such as fear, anger, shame or guilt, which is converted into a physical expression (Freud, 1953).  As a result, the patient actually reflects a symbolic solution to the same unconscious psychological conflict (Freud, 1953), which is supported by Heruti, Levy, Adunski and Ohry’s (2002, p.329) statement: “Freud accentuated the symbolic relation existing between the patient and the conflict”.  As well, Freud saw that there were primary and secondary gains for a patient to demonstrate symptoms of conversion disorder.

The primary gain was that “the anxiety produced by an internal unconscious defensive mechanism is converted into symbolic physical symptoms, while the conflict remains limited within the unconscious, thus resulting in the reduction of the anxiety level” (Heruti et al., 2002, p. 329).  Furthermore, Freud’s earlier opinion was that developing hysteria was characteristic of a person being dramatic, exhibitionistic, narcissistic, seductive, manipulative and dependent (Sethi & Lal, 2009).  However, this view is no longer held as these observations are considered to be broad generalizations, since they neglect social, cultural and spiritual factors.

There are alternative understandings of CD.  Freud’s French contemporary, Janet, conceptualized hysteria as a dissociative disorder and described somatoform symptoms as aspects of this condition in his traumatized patients (Sar, Akyuz, Kundakci, Kiziltan & Dogan, 2004).  In Janet’s opinion, the main basic disturbance of conversion disorders is “a weakening of the ability to perform cognitive or psychic synthesis causing the narrowing of the field of personal consciousness” (Buhler & Heim, 2011, p. 284), therefore, impairing personal consciousness.  Janet proposed a diathesis-stress-trauma model of conversion disorders whereby stress or trauma triggers emotions, which affects a patient’s fixed ideas (Buhler & Heim, 2011).  For the patient with conversion disorder, he/she will not have the ability to deal with the psychic tension and his/her personal consciousness is impaired.  Not only is the personal consciousness weakened, but it has a dissociative quality.  The patient is able to “encompass only a limited number of sensations and ideas and less able to control itself” (Buhler & Heim, 2011, p. 285).

Lastly, Janet (1989) understood the impairment of consciousness as the cause of dissociative anesthesia and a dissociation of psychic phenomena.  Janet viewed the basic disturbances of conversion disorder to be the proof of a weakening and exhaustion of the central nervous function.  In Janet’s perspective, the phenomenon should be viewed according to circumstances, not a character flaw and it is not judged to be either negative or positive.  In his viewpoint, this impairment belonged to coping, adjusting and adapting to stressful, traumatic circumstances (Janet, 1989).  The main focus of Janet’s stress-diathesis-trauma model brings new interest in the discussion of the categorization of conversion disorder, particularly as it has become more relevant and evident in several cultures.  Studies conducted on individuals from India have emphasized the role of stressors in conversion disorder (Sridhar & Sudharkar, 1997).  Furthermore, a study by Assam Medical College and Hospital found that school and family related stressors were significant precipitating factors for patients with conversion disorder (Deka, Chaudhury, Bora & Kalita, 2007).  Shalev and Munitz (1986) argue that symptoms of conversion disorder can be related to post-traumatic stress disorder.  These studies support Janet’s theory and conceptualization of this disorder as a dissociative disorder.

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The study by Brown and Lewis-Fernandez (2011) found that cross-culturally, conversion disorder is associated strongly with both dissociative and somatoform presentations.  Thus, the classification and understanding of the etiology greatly affects how we gather prevalence and characteristic data.  In different countries, certain symptoms and features were more prominent.  For instance, in Holland, motor disturbance, particularly paralyses, pareses and coordination disorders are central symptoms of CD (Brown & Lewis-Fernandez, 2011), whereas in Turkey, the loss of consciousness was identified as the most frequent symptom (Brown & Lewis-Fernandez, 2011).  Feelings of heat and “peppery” sensations were most common in Nigeria, India, Pakistan, and Nepal (Brown &Lewis-Fernandez, 2011, p. 45).

Studies conducted on Hispanic patients with multiple pseudo-neurological symptoms are more likely to report other symptoms characteristic of ataque de nervios than non-Hispanic patients reporting similar numbers of pseudo-neurological complaints (Brown & Lewis-Fernandez, 2011).  This supports the notion that patients with pseudo-neurological symptoms present differently, depending on their cultural origins and their associated representations of illness and well-being (Brown & Lewis-Fernandez, 2011).  According to these researchers, the argument to re-label conversion disorder in the dissociative disorder category is the result of the high co-morbidity between dissociative and conversion disorder symptoms.  On the other hand, proponents of retaining the category as a somatoform disorder, prioritize the co-morbidity between pseudo-neurological symptoms characteristic of conversion disorder and functional somatic symptoms.

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Lastly, the theoretical framework of social learning theory by Bandura offers a different but relevant manner of conceptualizing conversion disorder for cultures like India.  Role modeling has been reported in conversion disorder in some earlier studies (Sridhar & Sudharkar, 1997).  This perspective follows Bandura’s learned behavior principle of social modeling. Bandura contends that human behavior is largely influenced by the environment and personal factors (Bandura, 1977).  Patients may be modeling the coping mechanism they see from their family members, particularly from their role models such as their elders and parents (Sridhar &Sudharkar, 1997).  Furthermore, patients will express their feelings in a socially expected manner.  Response consequences of a behavior are formed by the expectations of the outcomes (Bandura, 1977).  The Indian culture, being one  where family members are more likely to respond to organic illnesses than psychological ones, it is most likely that people  manifest physical symptoms to illustrate their psychological symptoms (Syed, Effendi & Mehmud, 2011).  Researchers such as Deka, Chaudhury, Bora and Kalita (2007) explain that the role modeling theory is very plausible in India and has been highly reported in conversion disorder studies as it is common for these patients to unconsciously model their symptoms to those of someone important to them.

International studies (Syed et. al, 2011) suggest that although these symptoms may have low incidence rates in North America, they indicate that the current nosology used in DSM V and ICD-10 does not completely cover all aspects of this illness in various parts of the world.  They suggest that a separate category within the framework of conversion disorder needs to be introduced; otherwise, the majority of patients with conversion disorder would remain uncategorized due to atypical presentation.  Other researchers have similar suggestions.  Stone, Lafrance, Brown, Spiegel, Levenson & Sharpe (2011) suggested adding a criterion requiring clinical findings of internal inconsistency or incongruity.  They recommend the subsequent three changes for the new DSM V:

  1. “abandoning the label “conversion disorder” and replacing it with an alternative term that is both theoretically neutral and potentially more acceptable to patients and practitioners;
  2. relegating the requirements for “association neurological or medical disease and altering the current ‘disease exclusion’ criteria to one in which the symptom must not be ‘better explained’ by a disease, if present;
  3. adding a ‘cognitive symptoms’ subtype of  psychological factors” and the “exclusion of feigning”.

(Lafrance, Brown, Spiegel, Levenson & Sharpe , 2011, p. 372 )

In summary, the etiology of conversion disorder, whether it is Freud’s, Janet’s or Bandura’s theories, sheds light on how to explain this complex disorder, but adds to the complicated question of how to categorize conversion disorder.  Cultural variations of this disorder should not be brushed aside as post hoc since they are very much a part of the symptoms of this disorder.  Changes to our understanding of the conversion disorder whether is it a dissociative or somatoform disorder can help in the understanding of the etiology debate and assist in better diagnosing this disorder and making a differential diagnosis.

It’s been long known that anxiety and stress cause an increase in activity in the fear center of the brain (the amygdala and other parts of the brain) and a decrease in activity in the executive function parts of the brain (the prefrontal cortex and others).

However, this is the first time brain scans have been used to examine how emotion-regulation circuits are changed by anxiety and chronic stress in children.

The takeaway, however, is not that the brain is malfunctioning or damaged in some way due to anxiety, but that the brain is responding the way it’s supposed to when we think we are in danger. This change in brain function is an integral part of the body’s survival mechanism.

We explain this change in brain function in more detail in our “Stress Response” article.

We can remedy this change by behaving calmly instead of anxiously. As we use calming behavior, the executive function parts of the brain increase in activity, and the fear center decreases. Thus, restoring our ability to regulate our emotions.

So, it’s not that we can’t regulate our emotions when we’re anxious, but a matter of learning how so that we can gain more control over our emotions when we are anxious.

Recovery Support members can read the articles “Hyperstimulation And Its Effects,” “The Rational Brain And The Emotional Brain,” and the “Natural Ways To Shift The Body Out Of ‘Emergency Mode’” in chapter 14 for more information about how anxiety changes brain function and how to regain emotional control.

You can read the press release about this research below:

Stanford study finds stronger one-way fear signals in brains of anxious kids

Signals from the brain’s fear center make it more difficult for anxious and stressed children to regulate their emotions, a first-of-its-kind brain scanning study from Stanford shows.

In chronically stressed or anxious children, the brain’s fear center sends signals to the decision-making part of the brain that make it harder to regulate negative emotions, according to new research from the Stanford University School of Medicine.

The findings, which was published April 21 in Biological Psychiatry, come from the first study to use brain scans to examine how emotion-regulation circuits are changed by anxiety and chronic stress in children. The children studied were 10 or 11 years old, a developmental stage when vulnerability to mood-regulation disorders, such as anxiety and depression, becomes entrenched.

The study used functional magnetic resonance imaging to examine the nature of the signals between two parts of the brain: the amygdalae, almond-shaped nerve clusters on the right and left sides of the brain that function as its fear centers; and the dorsolateral prefrontal cortex, a brain region involved in executive functions such as decision making and emotion regulation.

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“The more anxious or stress-reactive an individual is, the stronger the bottom-up signal we observed from the amygdala to the dorsolateral prefrontal cortex,” said the study’s senior author, Vinod Menon, PhD, the Rachael L. and Walter F. Nichols, MD, Professor and professor of psychiatry and behavioral sciences. “This indicates that the circuit is being hijacked in more anxious children, and it suggests a common marker underlying these two clinical measures, anxiety and stress reactivity.”

Victor Carrion, MD, a co-author of the study and professor of child and adolescent psychiatry, said, “This study shows that the communication between our emotional centers and our thinking centers becomes less fluid when there is significant stress. You want that connection to be strongly signaling back and forth. But stress and anxiety of a certain level seem to interrupt that process.”

Carrion is the director of the Stanford Early Life Stress and Pediatric Anxiety Program, and is the John A. Turner, MD, Endowed Professor for Child and Adolescent Psychiatry. Lead authorship of the paper is shared by researcher Stacie Warren, PhD, and postdoctoral scholar Yuan Zhang, PhD.

Kids react to images

The study included 45 students in a California community with predominantly low-income residents who often face high levels of adversity. All 45 children had their anxiety levels and stress responses measured using standard behavioral questionnaires. Although their exposure to stress was potentially high, none were diagnosed with mood disorders.

To test how the children’s brains responded as they were trying to regulate negative emotions, the scientists conducted functional MRI scans while the study participants looked at two types of images, neutral and aversive. Neutral images showed pleasant scenes, such as someone taking a walk, whereas aversive images showed potentially distressing scenes, such as a car crash.

The children received instructions about responding to each image. For all the neutral images and half the aversive images, they were asked to look at them and respond to them naturally, rating their emotional state on a numerical scale after seeing each one. They were asked to look at the other half of the aversive images and try to reduce any negative reactions they had by telling themselves a story to make the pictures seem less upsetting — a story such as, “This car crash looks bad, but the people in the vehicles weren’t hurt.” After the kids tried to modify their emotional reaction, they again rated their emotional state on the numerical scale.

As the researchers expected, the children reported less negative emotions after being asked to reappraise their reactions to aversive images.

Using the brain-scan data, the researchers tested the strength and direction of interactions between the amygdala, the fear center, and the dorsolateral prefrontal cortex, the reasoning center, while the children viewed the images. Although the children with different levels of anxiety and stress reactivity reported similar reductions in their negative emotions when asked to reappraise the aversive images, their brains were doing different things.

More stress leads to less control of emotional reaction

The more anxious or stressed the child, the stronger the directional signals from the right amygdala to the dorsolateral prefrontal cortex. No such effects were seen in the reverse direction — that is, there was no increase in signaling from the dorsolateral prefrontal cortex to the amygdala. Higher levels of anxiety were associated with less positive initial reactions to aversive images, less ability to regulate emotional reaction in response to aversive images, and more impulsive reactions during reappraisal of aversive images. Higher stress reactivity was linked with less controlled, more impulsive reactions when reappraising aversive images, suggesting that the dorsolateral prefrontal cortex is less able to carry out its job.

Not only do the findings reveal how the brain can be changed by anxiety, they also act as a baseline for future studies to test interventions that may help children manage their anxiety and stress responses, the scientists said.

“We need to be more mindful about intervening,” Menon said. “These results show that the brain is not self-correcting in anxious children.”

“Thinking positively is not something that happens automatically,” Carrion said. “In fact, automatically we think negatively. That, evolutionarily, is what produced results. Negative thoughts are automatic thoughts, and positive thoughts need to be practiced and learned.”

The paper’s other Stanford co-authors are former research assistants Katherine Duberg and Sarah-Nicole Bostan; postdoctoral scholar Percy Mistry, PhD; Weidong Cai, PhD, clinical assistant professor of psychiatry and behavioral sciences; former postdoctoral scholar Shaozheng Qin, PhD; and former staff researcher Aarthi Padmanabhan, PhD.

This work was completed in partnership with the Ravenswood City, Alum Rock and Orchard school districts and Pure Edge Inc., which provides mindfulness curricula for children, and supported by the Lucile Packard Foundation for Children’s Health, the National Institutes of Health (grants EB022907, NS086085 and MH121069), the Stanford Maternal Child Health Research Institute and the Stanford Institute for Computational & Mathematical Engineering.

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