Article Title: Conversion Disorder

Author: Abdallah Aljabeiti

Editor: Rama Qatarneh

Keywords: Conversion Disorder, Functional Neurological Disorder , Hysteria

Introduction

Conversion disorder (CD), or more appropriately functional neurological symptom disorder (FNSD), is a psychiatric disorder characterized by the onset of sensory, motor, or cognitive symptoms that are not compatible with a known neurological disorder. It falls under the wider category of Somatic Symptom and Related Disorders. CD used to be a diagnosis of exclusion by having to rule out numerous neurological conditions, but as per the Diagnostic and Statistical Manual of Mental Disorders, 5^th edition (DSM-5), the diagnosis of CD now depends on the identification of positive findings to demonstrate preserved neurological functioning (1).

 

History of Conversion Disorder

Before being called conversion disorder, the sudden onset of severe neurological deficits without an obvious cause was referred to as hysteria. Hysteria was a colloquial term used to refer to emotional excess as a pathology and back then encompassed multiple conditions (that are now their own distinct diagnoses) including epilepsy, histrionic personality disorder, dissociative disorders, and conversion disorder (2,3).

The oldest accounts of hysteria date back to 1900 BC where the Egyptians documented cases of abnormal behavior in women on medical papyrus. Among multiple theories, one theory attributed these behavioral abnormalities to a ‘wandering’ dried-up uterus that traverses the body in search of moisture. Subsequently, the allegedly wandering uterus could lodge itself in other areas and compress certain structures causing disease, one of which is hysteria. Egyptian doctors believed that treating hysteria could be accomplished by inducing the uterus to return to its original position either by using strong-smelling substances on patients’ vulvas in an attempt to make the uterus return to its position or in other instances, smelling or swallowing unsavory herbs to encourage the uterus to ‘run’ back into position.

All of this of course implies that hysteria was a disease pertinent to females only, which was the prevailing idea at the time. Fast-forwarding to sometime between the 4^th and 5^th centuries BC in ancient Greece, the theory set forth by the Egyptians was originally accepted and thus named ‘hysteria’, from the Greek word hystera meaning uterus, as documented by Hippocrates (3). However, with the advancement of anatomy, the theory was abandoned. In ancient Rome, 2^nd century AD, Galen proposed a new theory where hysteria was thought to be caused by retention of uterine secretions. It is worth noting that Galen did acknowledge the presence of a similar disease in men, due to the retention of sperm (4).

Sometime between the 5^th and 13^th centuries of the middle ages, the focus of the etiology of hysteria was shifted from one of physical disease to one of satanic possession. Unsurprisingly, that meant hysterics were treated with prayers, amulets, and exorcisms. During the Renaissance period, many hysterics were prosecuted as witches, undergoing interrogations, torture, and execution (5). Some centuries later, around the 16^th-17^th centuries, there were advancements to restore hysteria back into the realm of medicine by many physicians including the French physician Charles Lepois and English physician Thomas Sydenham. Many physicians followed and hysteria became disassociated from the soul and the uterus (6).

Moving forward to the last 3 centuries, Sigmund Freud hypothesized that the etiology of hysteria and its symptoms were a reflection of unconscious conflicts and accordingly coined the term “conversion disorder” (7). However, researchers have not yet been able to find evidence supporting the notion of ‘conversion’ (8) and thus, the term ‘conversion disorder’ is carried forward to our day and time for the sake of preserving historic continuity (9). Many physicians now use CD interchangeably with FNSD or functional neurological disorders (FND), which omits any etiological inference of ‘conversion’ from the name.

 

Epidemiology

Conversion disorder is one of the most common causes of referral to neurological outpatient settings, only coming second to headaches (10,11). It is more common in women, especially those between the ages of 35 and 50 (12–14).

 

Etiology & Pathophysiology

Elucidating specific etiologies for the development of CD has been elusive, however, a constellation of psychological, social, and biological factors is thought to contribute to precipitating or perpetuating CD. These include trauma, adverse life events, acute/chronic stressors, and childhood abuse (emotional/sexual). Other intrinsic factors include poor coping skills and internal psychological conflicts (15). Video electroencephalography (EEG) telemetry and high-resolution structural neuroimaging have shown that even in the presence of the most disabling symptoms in the CD context, there is no structural pathology. Rather, a functional defect was demonstrated on functional neuroimaging and neurophysiology (16). It is also worth noting that the presence of a traumatic experience is not necessarily a prerequisite to developing CD, it can be present but it is not the defining factor, hence the predilection to call CD more appropriately as a functional neurological disorder rather than one of a ‘conversion’ etiology (1).

 

Risk Factors

Risk factors for CD include early life stress (whether in the form of childhood abuse or neglect), stressful events, having maladaptive personality traits, and the presence of a neurological disease that causes similar symptoms (1,17,18).

 

Clinical Presentation

Before delving into the presentation of CD, it is important to note that the symptoms and signs are not controlled at will and are not being feigned by the patient (7). CD can present with many different symptoms, so presentations can vary widely (19). The dysfunctions in CD are alterations in sensory, motor, or cognitive function. Sensory dysfunction can present as anesthesia or sensory loss, visual, hearing, or olfactory disturbances. Motor dysfunction presents as weakness, paralysis, abnormal movements (tremors, myoclonus, dystonic movements), seizures, gait abnormalities, or dysfunction in swallowing or speech. The most common presentations include weakness/paralysis, abnormal movements, seizures, swallowing/speech dysfunction, visual disturbances, and syncopal episodes (20). Some patients also present with a paradoxical absence of distress despite having serious symptoms known as “la belle indifference”. It is not specific for CD, and is not required for diagnosis but is nonetheless observed in a subset of patients (1,21,22).

In children, the presentation is usually monosymptomatic with higher chances that the dysfunction is in the dominant extremities (23–25).

The tables in Figure 1 and Figure 2 detail how the sensory and motor dysfunctions present and how to differentiate their occurrence in CD from their occurrence in neurologic disorders (26).

 

Diagnosis

The criteria for diagnosis by the DSM-5 are as follows (1):

1. ≥ 1 symptom(s) of voluntary motor or sensory dysfunction
2. Discrepancy between the features of the symptom(s) experienced and recognized neurological/medical conditions
3. The presentation is not better explained by another medical/mental condition
4. The symptom(s)/deficit(s) cause significant distress or impair aspects of daily functioning (occupational/social/etc.) or require medical attention

Specifiers include:

• Specifying the symptom type: with weakness/paralysis, abnormal movement, swallowing symptoms, speech symptoms, attacks/seizures, anesthesia/sensory loss, special sensory symptoms (visual/olfactory/hearing), or mixed symptoms
• Specifying the duration: considered an acute episode if the symptoms are present for < 6 months, and persistent when the symptoms persist for ≥ 6 months
• Specifying the presence/absence of a psychological stressor

 

Differential Diagnosis

Although the diagnosis of CD requires the symptoms to not be better explained by another condition, that does not exclude the possibility of diagnosing CD with the presence of another condition depending on how the patient presents. The differential diagnosis for CD includes the following (1):

• Neurological disorders: multiple sclerosis, strokes, Guillain-Barré syndrome, myopathies, polymyositis, and myasthenia gravis can have similar presentations to CD (32). This however doesn’t mean a neurological disorder can’t also be comorbid with CD (26)
• Somatic symptom disorder (SSD): CD often lacks the excessive thoughts, feelings, and behaviors that characterize SSD
• Factitious disorder and malingering: the diagnosis of CD does not require explicit proof that the symptoms are not being feigned, due to the difficulty and unreliability of assessing conscious intentions. However, in the presence of definite proof of feigning (e.g., demonstrating symptoms and signs during examinations whilst not having symptoms/signs at home), the alternate diagnoses of factitious disorder or malingering need to be considered
• Dissociative disorders: dissociative symptoms (depersonalization/derealization/etc.) can be present in CD
• Depressive disorders: patients with depressive disorders can report a general sensation of heavy limbs, not to be confused with the weakness that a CD patient might present with
• Panic disorder: tremors and paresthesia can present in both panic disorder and CD, but are more transient and associated with characteristic cardiorespiratory symptoms in panic disorder
• Body dysmorphic disorder

 

Complications and Comorbidities

Complications include an impaired quality of life and a chance of permanent disability. The level of impairment and psychological/physical disability in CD can be compared with or even be shown to be higher in some instances than actual neurologic diseases (26).

CD patients are also more likely to have comorbid mental illnesses than those with neurologic diseases. Most notably depressive disorders, anxiety disorders, PTSD, personality disorders, dissociative disorders, and illness anxiety disorder (15,33–37).

 

Treatment

The treatment for CD is a multidisciplinary one, and mainly involves appropriate delivery of the diagnosis to the patient, reassurance, and psychotherapy. The treatment plan could also include occupational and physical therapy or pharmacotherapy.

Delivery of the diagnosis and reassurance

Effective presentation of the diagnosis to the patient is quite possibly the most important aspect of treatment (32). Many patients have negative experiences during their care-seeking period, due to both poor knowledge of CD and the tendency for some clinicians to discredit the patients’ experiences and attribute symptoms to something that is “all in their head” whether it is implied or explicitly stated (38,39). It is also recommended that the physician maintain a strong patient-physician relationship before revealing and explaining the diagnosis. It is very important to acknowledge that the patient’s symptoms are real and show empathy towards how the patient’s life is being adversely affected. Another aspect is explaining the diagnosis to the patient adequately and explaining to the patient how the diagnosis was reached (e.g., by pointing out the differences in history and physical exam that helped differentiate between organic disease and CD). It is also important to explain that the symptoms being experienced are possibly reversible if the patient adheres to the treatment plan (32).

Psychotherapy

Psychotherapy is considered to be the first-line treatment in most cases. The most effective one being cognitive-behavioral therapy (CBT). Other classes of psychotherapy can be employed, such as psychodynamic psychotherapy, group therapy, family therapy, and hypnotherapy (40,41). Hypnotherapy is especially useful as a second-line treatment in patients with speech symptoms or sensory loss (26), the first-line treatment for speech symptoms being speech therapy (42).

Pharmacotherapy

Pharmacotherapy is not considered a main line of therapy, however, its role becomes more pronounced in the presence of comorbid mental conditions. The choice of drug depends on the comorbidity, but it can include antidepressants, anxiolytics, or mood stabilizers. Several studies evaluated the effects of antipsychotics, and it was found that quetiapine and haloperidol had comparable effects in alleviating symptoms (32,43).

Occupational and physical therapy

Patients with functional motor symptoms (weakness/paralysis) can especially benefit from physical or occupational therapy sessions to encourage normal movement and reinstate motor function back to the baseline or a comparable state (26,44–46). Patients with speech dysfunction can benefit from speech therapy sessions to regain normal speech (42).

 

Prognosis

Prognosis relies on many factors, but generally, it is poor. Positive prognostic factors are early diagnosis, short duration of symptoms, lack of comorbidities (especially personality disorders), identifiable stressors, and a positive patient-physician relationship. Negative prognostic factors include greater number of physical symptoms, poor physical functioning prior to diagnosis, and maladaptive personality traits (1,7,26). Children have better outcomes and usually experience complete resolution of symptoms within 3 months of diagnosis with rare chances of recurrence (1,47–49).

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