New approaches to conversion hysteria
BMJ 2000; 320 doi: https://doi.org/10.1136/bmj.320.7248.1488 (Published 03 June 2000) Cite this as: BMJ 2000;320:1488
Functional imaging may improve understanding and reduce morbidity
- Peter W Halligan, MRC senior research fellow,
- Christopher Bass, consultant in liaison psychiatry,
- Derick T Wade, consultant in neurological disability
- School of Psychology, University of Cardiff, PO Box 901, Cardiff CF1 3YG
- Department of Psychological Medicine, John Radcliffe Hospital, Oxford OX3 9DU
- Rivermead Rehabilitation Centre, Abingdon Road, Oxford OX1 4XD
Patients with hysterical conversion, now called conversion disorder by the main US psychiatric glossary,1 often present with striking neurological symptoms such as weakness, paralysis, sensory disorders, or memory loss, in the absence of any pathology that could be responsible. Most patients will be referred to a neurologist or psychiatrist after consulting their family doctor.
As many as 4% of those attending neurology outpatient clinics in the United Kingdom have been estimated to have conversion disorders.2 Similar rates have been reported for both in and outpatient clinics in other European countries.
Empirical research on hysterical conversion has lagged behind theoretical speculation. Recent advances in functional imaging (positron emission tomography scanning) and cognitive neuropsychology have, however, made the field more amenable to investigation.3 Key clinical and theoretical problems remain over case definition and differential diagnosis, the psychological mechanisms underlying conversion hysteria, and how patients are best managed.
Despite attempts over the past century to abolish and reinstate the condition by using different labels, conversion hysteria continues to attract controversy.4 5 The diagnosis is considered pejorative, and its place within psychiatric classification remains uncertain. There is no generally accepted explanation for how a psychological stress can convert into (often highly selective) symptoms. In this respect, conversion hysteria retains “the doubtful distinction among psychiatric diagnoses of still invoking Freudian mechanisms as an explanation.” 6
The diagnosis of conversion hysteria is typically made after excluding organic pathology and identifying a relevant psychological stressor. Problems with diagnosis include the extent to which organic disorders can and should be excluded; agreement on what constitutes relevant psychological conflict; and the criteria used to exclude malingering.
Technology reduces the risk of missing organic disease
There are few, if any, empirical data to support the diagnostic criteria given in psychiatric glossaries, and in clinical practice intuition and experience play a large part in the diagnosis. There is little evidence to determine what constitutes a relevant psychological stressor. A recent study, however, showed that the use of modern technology minimised the likelihood of missing organic disease.7 It is likely that particular people may be at risk because of some underlying vulnerability. Evidence for this may prove difficult to find, and it remains impossible to exclude malingering as a potential cause.
For much of this century the search for the neurological systems responsible for conversion hysteria was largely ignored. The crux of the problem is to explain how abnormal psychological states can produce specific, long term neurological symptoms and disability in patients (who claim not to be consciously responsible) in the absence of detectable pathology.4
Recent evidence from functional imaging provides some indication of the possible brain areas involved. The functional imaging study by Marshall et al of a patient with left sided paralysis (but with no detectable lesion) found that when the patient tried to move her affected limb, considerable activity was seen in the right anterior cingulate and orbitofrontal cortex.8 These activations were identified as the prefrontal structures responsible for inhibiting the patient's volitional movements.
To bridge the gap left by the traditional overreliance on psychodynamic theory, several neuropsychological accounts have emerged.3 Instead of trying to explain conversion hysteria, these are more concerned with working out how impairments to normal cognitive processes such as volition, memory, and motor and sensory control may cause clinical symptoms.9
The conceptual link between hypnosis and hysteria has also been highlighted. Particularly in the acute stage, conversion symptoms and hypnotic phenomena share many features, to the extent that experiments on hypnosis (considered a kind of controlled hysteria) have long served as experimental analogues for the study of hysterical symptoms. The view that conversion symptoms can be usefully thought of as an autosuggestive disorder gains some support from a recent functional imaging study by Halligan et al, which showed that the areas of the brain activated by paralysis induced by hypnosis are similar to those activated in hysterical paralysis.8 10 11
There have been no controlled studies of treatment of patients with conversion hysteria. The uncontrolled case reports and series that exist are difficult to evaluate, as some patients improve spontaneously and the psychological benefits of any intervention may be more important that the specific intervention.
The lessons learnt in the treatment of chronic fatigue syndrome and other somatoform disorders may be applicable.12 There is potential in using a cognitive behavioural approach, avoiding reinforcement of the abnormal illness behaviour, and facilitating more appropriate links between life situations and physical symptoms. Life events and social circumstances can dramatically change a person's prognosis, and there is emerging evidence that patients who experience a change in circumstances and life events after the onset of their symptoms have improved outcomes.13
Evidence is building that although conversion hysteria causes major disability, it is almost certainly not a disease with a specific pathology. Although the diagnosis carries a negative connotation for patient and doctor, its aetiology and management deserve further study.
Whether new developments in functional imaging and cognitive neuroscience can move the debate beyond disputes about how the disorder should be classified to testable hypotheses about the neuropsychological and social mechanisms involved in the disorder remains to be seen.