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CONVERSION DISORDER- THE MODERN

CONVERSION DISORDER- THE MODERN HYSTERIA

Nemowtee Anita Ramdinny1Dr Netranee Anju Ramdinny-Purryag 2

1Master Curriculum, 2Psychiatrist

Consultant Jeen pharmacy Mauritious

Abstract

People with conversion disorder develop unexplained symptoms or losses in function that are judged to stem from psychological conflicts. Described as early as 1900 B.C, the symptoms or deficits in conversion disorder tend to occur suddenly and involuntarily and typically affect just a single body function.1

Information on the prevalence of conversion disorder in the West is limited, in part due to the complexities of the diagnostic process. In neurological settings, rates of unexplained symptoms are very high, between 30-60%,2 which suggests conversion to be more common than most neurological diseases. Large scale psychiatric registers in the Unites States and Iceland found rates of 22 and 11 per 100,000 per year respectively, 3 but it is unclear what proportion of unexplained symptoms these represent.

A community survey of urban Turkey found a prevalence rate of 5.6%.4 Many authors have found rates to be higher in rural and lower socioeconomic groups 3.‘Hysteria’ was originally understood to be a condition exclusively affecting women, though it has increasingly been recognised in men. In recent studies, women continue to predominate, with between 2 and 6 female patients for every male.2,4 Conversion disorder may present at any age but is rare in children younger than 10 years or in the elderly. Studies suggest a peak onset in the mid to late 30s.2,3,4

 

Conversion disorder in India

Hysteria patients constitute a major proportion of psychiatric patient population in developing countries.5 Some Indian studies have focused on the clinical characteristics  in conversion disorder.6 They have emphasized the role of stressors in conversion disorder. “Role model” has been reported in conversion disorder in some earlier studies. A role is an automatic learned, goal-directed pattern or sequence of acts developed under the influence of significant people in a growing child’s environment. Patients with conversion disorder may unconsciously model their symptoms in those of someone important to them. In India, high occurrence of conversion disorder has been reported in young adults, from poor low-income, joint families and significantly higher in females.7 Also, higher prevalence has been seen in illiterates, married housewives being the largest group.8

 

The Psychiatric History and theories of Conversion Disorder

That it is still helpful or even necessary to review historical models of the disorder reflects our lack of progress in confirming or refuting these models. The puzzle of hysteria, as it was previously known, had been documented for millennia but only began to assume its current form in the 19th century. Although physicians as far back as Willis had previously taken a psychological view of hysteria and others had considered it to be malingering, the debate crystallized with the development of post-mortem neuropathology whereby many other neurological disorders were found to have distinct anatomical and cellular abnormalities. The absence of pathology led Char cot to use the term ‘functional’ to describe conversion disorder and other ‘neuroses’ such as migraine, where no pathology was demonstrable but in which function was clearly disturbed, concluding that there must be a ‘dynamic lesion’. This countered the view that its anomalous nature could best be explained by feigning, and so, as Freud later put it, restored ‘dignity’ to the topic although Charcot’s particular model did not survive for long after his death.

Psychological theories of conversion disorder were increasingly found in neurological thinking in the mid to late 19th century but it was not until the models of Freud and Janet that they prevailed. Pierre Janet proposed that ‘dissociation’ could explain the symptoms as a defect in the psychological constitution. He suggested that dissociation could lead to problems maintaining the normal conscious synthesis of experiences: ‘a special moral weakness, consisting of the lack of power, on the part of the feeble subject, to condense his psychological phenomena and assimilate them to his personality.’ He proposed that under a variety of conditions, including trauma, a rogue ‘idea’ such as that of a weak limb, could become fixed and separated from the consciousness that was too weak to exert control over it.

Freud proposed a different mechanism in which unwelcome experiences are ‘repressed’ into the unconscious but in doing so become converted into physical symptoms: ‘she repressed her erotic idea and transformed the amount of its affect into physical sensations of pain.’ Freud argued that although the repression was deliberate, in order to escape from distress (which he called primary gain), the conversion was not: ‘The splitting of the consciousness... is accordingly a deliberate and intentional one....the actual outcome is something different from what the subject intended.’ “Secondary gains” could also accrue as the resulting physical symptoms enabled escape from conflicts or other unwanted outcomes- for example, paralysis stopping a partner leaving or resulting in more attention from a significant other. Freud later revised his view to argue that these traumas were only so debilitating because they awakened memories of childhood sexual abuse and then dropped the latter idea in favour of his theory of infantile sexuality. Although he subsequently revised this view again, those early ideas of repression, conversion and sexual abuse come to dominate post-Freudian psychiatric models of hysteria.9,10

The acceptance of these models changed hysteria from a neurological condition akin to migraine into a purely psychiatric disorder. Over the 20th century, psychiatrists embraced the condition even as they noted its apparent disappearance from their clinics.11 Hysteria entered the diagnostic classification, with terminology that embodied the dominant Freudian model- conversion hysteria in the latter part of the century. As enthusiasm for biological psychiatry grew, in the UK in particular, there were moves to a more neutral model12 and the term dissociation, still in common use in psychological circles, re-entered the nomenclature in ICD-10, describing ‘dissociative seizures’ and becoming a synonym in ‘dissociative (conversion) disorder’.

 

Causes

Episodes of conversion disorder are nearly always triggered by a stressful event, an emotional conflict or another mental health disorder, such as depression. The exact cause of conversion disorder is unknown, but the part of the brain that controls muscles and senses may be involved. It may be the brain’s way of coping with something that seems like a threat.

The old term for conversion disorder was hysteria. Physicians in ancient Greece believed that hysteria occurred in females and that it was caused by the uterus wandering in the body (the greek word for uterus is hysteria). For centuries thereafter, people with hysteria were regarded as fakers or imagining their symptoms. In the 17th century, some people with hysteria were thought to be involved with witchcraft and were burnt at the stake.

The term conversion disorder came into use only in the 20th century. It is derived from the early work of the Australian physician Sigmund Freud, the founder of psychoanalysis.

Freud believed that in times of extreme emotional stress, painful feelings or conflicts are repressed (kept from awareness or consciousness) and are converted into physical symptoms to relieve anxiety. Even in the 21st century, mental health experts do not all agree on the precise psychological mechanisms underlying conversion disorder. However, many mental health professionals see the benefits associated with the symptoms of conversion disorder, such as sympathy, care and the avoidance of stressful situations, as significant to the disorder.

Conversion symptoms are more common among the uneducated and unsophisticated, the actual conversion symptom itself is generally a reflection or extension of symptoms that the patient has seen in another or has personally experienced.

In most instances, consequent upon the appearance of the conversion symptom, there is a reduction in the patient’s level of anxiety. Close inspection reveals that conversion symptoms are not, however, premeditated; they simply happen – and although observers may feel a “purpose” is behind them, the patient himself is unaware of any such thing. Many clinicians feel that the symptoms itself may be a kind of sign language or a sort of hieroglyphic that conveys what the patient is unable to put into words.

Recent PET scanning has demonstrated that in patients with conversion hemiplegia or hemianaesthesia, there is a decreased activation of the contralateral basal ganglia and thalamus.13 The pathophysiologic relevance of this finding, however is unclear. It may represent a premorbid susceptibility to the development of conversion symptoms or might, in turn, merely be epiphenomenal and unrelated to the underlying cause or causes.

 

Controversy about the cause

Around 25% of conversion disorder patients are later diagnosed with authentic medical ailments that account for their symptoms. The complexity of conversion disorder is magnified by the fact that genuine illness and conversion disorder can co-exist. Sometimes, for instance, patients with genuine epilepsy have conversion seizures as well. In a true grand mal seizure, a patient has massive electrical discharges from all parts of his or her brain, leading the body jerking and tongue biting. In conversion disorder on the other hand, the patients have normal brain activity even when they appear to be in throes of a seizure.

 

Clinical Features

Conversion disorder can present with any motor or sensory symptom including any of the following:

1.       Weakness/paralysis of a limb or the entire body (hysterical paralysis or motor conversion symptoms)

2.       Impaired vision (hysterical blindness) or impaired hearing.

3.       Loss/disturbance of sensation

4.       Impairment or loss of speech (hysterical aphonia)

5.       Psychogenic non-epileptic seizures

6.       Fixed dystonia unlike normal dystonia

7.       Tremor, myoclonus or other movement disorders

8.       Gait disturbances (astasia-abasia)

9.       Syncope (fainting)

10.   Hallucinations of a childish or fantastic nature

11.   Tourette-like symptoms

 

Mass Psychogenic Illness

DSM-IV TR does not have a specific diagnosis for mass psychogenic illness but the text describing conversion disorder states that in ‘epidemic hysteria’, shared symptoms develop in a circumscribed group of people following exposure to a common precipitant.

 

Course

Conversion disorder may pursue either an episodic or chronic course, with the initial conversion symptom remitting spontaneously, often within weeks or months. In such cases, a subsequent episode may be expected in the years to come. Should such a subsequent episode occur, the conversion symptom itself may be different from the initial one.A minority of patients experience their conversion symptoms chronically; this tends to be the case with an associated personality disorder.

 

Complications

Should patients take to bed or restrict their activities because of conversion symptoms, jobs may be lost and relationships strained. Potentially dangerous diagnostic procedures, such as arteriography may be undergone. In chronic cases of conversion paralysis, disuse atrophy or contractures may occur.14

 

Treatment

After the diagnosis is made, one should inform the patient in a gentle and nonjudgmental, yet quietly authoritative way that neither the examination nor the diagnostic tests have revealed any damage to the brain or nerves. One may then confess honestly that, although medicine does not know the cause of the symptoms, it is nevertheless known that patients tend to recover in a few weeks. With such support and reassurance, a majority of patients will experience a remission during a hospital stay and this is especially likely when the conversion symptoms have been of acute onset and short duration and were preceded by an obvious psychosocial precipitant. In certain instances, a few sessions with a physical therapist that is knowledgeable about these patients may expedite the remission, often providing a sort of “face-saving” device. At all costs, one must avoid pejorative statements such as “there is nothing really wrong with you” as these only serve to undermine the physician-patient relationship.

 

When these measures fail, alternative techniques may be used. Hypnosis may effect a remission; however early relapses tend to occur.15 Another approach involves viewing the symptoms as a kind of “sign language”, deciphering what the sign means and then assisting the patient in putting that meaning into words and taking appropriate action.16 Such an approach is often labour intensive, yet the clinical impression is that it may produce solid results.

Working with the family unit may be necessary when family and sociocultural factors predominate, particularly in children and adolescents. Family therapy interventions help the patient and family recognize and address key issues which may be fuelling the symptoms. For example, in an analysis of videotaped family interviews of adolescent patients, an unspeakable dilemma was imposed by family or social circumstances in 13 of 14 cases, leading patients with nonepileptic seizures to suppress emotional distress.17

Recognition and treatment of comorbid psychiatric conditions are almost always necessary for symptom resolution. If patients continue to be symptomatic after these risk factors have been addressed, then psychological treatments that focus more directly on perpetuating factors will be necessary. Patients’ reactions (and physicians) reactions to their conversion symptoms can serve to unwittingly perpetuate them. Avoidant behaviours, minimisation of psychological factors and suppression of expression of distress reinforce an external locus of control.  Cognitive behaviour therapy lends itself well to addressing these issues. It is specifically helpful in addressing illness beliefs and denial of stress and in modifying the locus of control.18

Psychodynamic psychotherapy can also serve to help patients reframe their world view through empathic interpretations and the development of insight, enabling the process of working through past trauma rather than on relying on dissociation as a defense. Both approaches will increase awareness of “triggering events”

 

Conclusion

Early recognition of a conversion disorder will limit unnecessary tests and medications. Long term benefit requires a comprehensive treatment approach, recognition of risk factors and treatment of comorbid conditions, with a focus on cognitive styles that perpetuate symptoms. The quality of the doctor-patient relationship can influence the outcome. Hard-to-treat patients may engender feelings of powerlessness, frustration and mistrust in their treaters, which if unprocessed may lead to a poor relationship and excessive use of medications, tests and procedures. There are few published reports on prospective studies or controlled trials of treatment for patients with nonepileptic seizures. The existing medical literature supports a multidisciplinary treatment approach, with specific interventions, such as cognitive behaviour therapy for cognitive restructuring and psychodynamic therapy for addressing symptom connections to trauma and dissociation. Adjunctive group therapy or family therapy works well for certain patients. Hypnosis can be beneficial, although it is not essential for a good outcome. Judicious medication treatment for comorbid disorders, alone or in combination is often needed for sustained therapy.

 

References

1.        Aybek S, Kanaan RA, David AS. The neuropsychiatry of conversion disorder. Curr Opin Psychiatry 2008; 21:275-280.

2.        Carson AJ, Ring BB, Stone J et al. “Do medically unexplained symptoms matter? A prospective cohort study of 300 new referrals to neurology outpatient clinics.” J Neurol Neurosurg Psychiatry 2000; 68(2): 207-10.

3.        Stefansson JG, Messina JA, Meyeronitz S. “Hysterical neurosis, conversion type: clinical and epidemiological considerations.” Acta Psychiatrica Scandinavia 1976; 53(2): 119-38.

4.        Deveci A, Taskin O, Dinc G et al. “Prevalence of pseudoneurological conversion disorder in urban community in Manisa, Turkey. Soc Psychiatr Epidemiol 2007; 42(11): 857-64.

5.        Wig NN, Mangal  WK, Bedi H, Murthy RS. A follow up study of Hysteria. Indian J Psychiatry 1982; 24:120-5.

6.        Mahli P, Singhi P. Clinical characteristics and outcome of children and adolescents with conversion disorder. Indian Paediatr 2002; 39: 747-52.

7.        Vyas JN, Bharatraj PK. A study of hysteria-AN Analysis of 304 patients. Indian J Psychiatry 1977; 19:71-4.

8.        Saxena S, Pachauri R, Wig NN. DSM-111 diagnostic categories for ICD-9 Hysteria: A study of 103 cases. Indian J Psychiatry 1986; 28: 47-9.

9.        Mace CJ. Hysterical Conversion: A history. Br J Psychiatry 1992; 161: 369-77.

10.      Gottlieb RM. Psychosomatic medicine: the divergent legacies of Freud and Janet. J Am Psychoanal Assoc 2003; 51: 857-81.

11.     Micale MS. On the “disappearance” of hysteria. A study in the clinical destruction of a diagnosis. Isis 1993;84: 496-526.

12.     Stone J, Henett R, Carson A et al. The “disappearance" of hysteria: historical mystery or illusion? J R Soc Med 2008; 101: 12-8.

13.     Vuilleumier P, Chicherio C, Assaf F et al. Functional neuroanatomical correlates of hysterical sensorimotor loss. Brain 2001; 124: 1077-1090.

14.     Baker AH, Silver JR. Hysterical paraplegia. Journal of Neurology, Neurosurgery and Psychiatry 1987; 50: 375-382.

15.     Moene FC, Spinhoven P, Hoogdwin KA et al. A randomized controlled clinical trial on the additional effect of hypnosis in a comprehensive treatment program for inpatients with conversion disorder of the motor type. Psychotherapy and Psychosomatics 2002; 71: 66-76.

16.      Speed J. Behavioural management of conversion disorder: retrospective study. Archives of Physical Medicine and rehabilitation 1996; 77: 147-154.

17.      Griffith JL, Polles A, Griffith ME: Pseudoseizures, families and unspeakable dilemmas. Psychosomatics 1998;39:144-153.

18.     Goldstein LH, Deale AC, Mitchell-O Malley SJ, Toone BK, Mellers JD. An evaluation of cognitive behavioural therapy as a treatment for dissociative seizures: a pilot study. Cogn Behav Neurol 2004; 17: 41-49.