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Functional MRI and transcranial magnetic stimulation data are helping to explain the aetiology of conversion disorder.
Conversion disorder occupies some unusual niches within the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).1 It is one of the very few conditions where the manual makes reference to aetiology, invoking emotional conflict or other stressors as an initiating or exacerbating factor in the symptom production. Furthermore, the typical symptoms of conversion disorder, like loss of sensation, paralysis or, as in the case reported by Chastan et al (see page 94), aphonia, are deemed “pseudoneurological.”2 It is for these reasons that conversion disorder is still regarded by the DSM-IV as quintessentially a psychological disorder even as psychiatry, embracing advances in neuroscience, abandons the outmoded concept of an organic–functional divide.
Chasten et al used repetitive transcranial magnetic stimulation (rTMS) applied to the motor cortex to treat a patient whose aphonia was considered a symptom of conversion disorder. The good response was not attributed to a placebo effect, given that prior stimulation of the left prefrontal cortex elicited no such improvement. Symptom resolution following a single rTMS treatment, still present after 6 months, was given added salience by the earlier failure of the patient to respond to 30 sessions of speech therapy. This dramatic result begs the question why rTMS proved so effective.
Here it is informative to step back in time. In 1886, the young Sigmund Freud, working as a neuropsychiatrist and on the cusp of defining psychoanalytic theory, turned his attention to conversion disorder, then called hysteria.3 Freud conceptualised the symptoms arising from what he termed a “large quota of affect.” Freud posited that excessive affect prevented the individual, at an unconscious level, from making appropriate associations—for example linking movement to an arm or sensation to a hand. In short, emotion could compromise the brain’s functional integrity.
Recent evidence from a small series of fMRI studies suggests this theory may have some validity. A reduction or absence in cerebral activation has been recorded in the motor and sensory cortices of patients presenting with the motor or sensory subtypes of conversion disorder, respectively. At the same time, these patients showed ancillary activations in the anterior cingulate and orbitofrontal cortex, regions that play a pivotal role in modulating emotion.4 5 What Chasten et al suggest is that rTMS has the ability to restore the appropriate cerebral connectivity by activating a suppressed motor cortex (or, for that matter, any other inactive cortical region) while presumably over-riding the inhibitory influence of an aroused limbic system.
This is an interesting theory, but further research is needed to replicate and extend the findings. The patient with aphonia in Chasten et al’s report did not have functional brain imaging. Therefore, a study that combines rTMS with a fMRI protocol pre- and post-treatment offers a robust way of putting theory to the test. And here, a note of caution seems prudent. Conversion disorder is a complex phenomenon. A reductionist theory positing a single aetiological mechanism, no matter how intriguing, is unlikely to provide all the answers. It is, however, a useful point of departure.
Competing interests: None.
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