Conversion Disorder

Blog Post by James J. Amos MD, University of Iowa, USA 

I was fascinated by the blog “The Mind in Modern Medicine” by E.S. Krishnamoorthy, et al, posted 10/21/2010. As a Psychosomatic Medicine (PM) specialist, I’m often consulted by neurologists for help managing hysteria, nowadays called conversion disorder. Although it’s been in the somatoform disorder category for many years, the opinion of many of my colleagues is that it’s more of a dissociative state. It may be reclassified in the next version of the Diagnostic and Statistical Manual (DSM-V). I’m always struck by the apparent faith my colleagues in Neurology have in the expertise of psychiatrists in the treatment of conversion disorder. In fact, there is scant evidence of efficacy for any specific psychosocial intervention(Lesley and Robert 2010). For example, one author has written of the clinical utility of using “abreaction” in the management of conversion disorder. The critical component is using suggestion, with or without a drug such as a barbiturate like sodium amytal, especially with treatment resistant conversion disorder(Poole, Wuerz et al. 2010). In fact that’s what I and many other psychiatrists commonly do for patients with conversion disorder— simply suggest the medically unexplained symptom will gradually resolve. Frequently, the vexing problem is the lack of opportunity for follow-up so that I can track outcomes. Some neurologists think of conversion disorder as a form of feigning(Kanaan, Armstrong et al. 2009). However, it’s intriguing that functional brain imaging such as SPECT scans demonstrates abnormalities including but not limited to selective diminution in frontal and subcortical circuit activity involved in motor control in hysterical paralysis. On the other hand, there is also increased activation in limbic regions, such as cingulate or orbitofrontal cortex during conversion symptoms. This moves us further toward a clearer understanding of not just the neuropsychobiological underpinnings of somatization, but of the brain mechanisms of self-awareness(Vuilleumier and Steven 2005).

Many psychiatrists wonder how we can reliably tell if someone is faking, somatizing, or has another psychiatric disorder which is driven by motivations that the patient is either unable or unwilling to share with us. That’s the problem with distinguishing between Factitious Disorder, malingering, and somatoform disorders. The inability to discern motivation may occasionally even interfere with distinguishing these disorders from catatonia or selective mutism. I’ve used C. Miller Fisher’s so-called telephone effect for temporarily reversing abulia to provoke patients who are apparently mute from catatonia into answering questions(Fisher 1983). Abulia and catatonia are very much alike clinically. This is a clever and sometimes dramatically effective maneuver that impresses trainees. One simply telephones a patient who is mute on direct interview from across the hall. They talk on the phone. I’m reasonably sure one of them who responded was not catatonic. Articles like Krishnamoorthy’s renew my excitement and hope for future collaboration between Psychiatry and Neurology in moving health care to the next level.

Fisher, C. M. (1983). “Honored guest presentation: abulia minor vs. agitated behavior.” Clin Neurosurg 31: 9-31. Kanaan, R., D. Armstrong, et al. (2009). “In the psychiatrist’s chair: how neurologists understand conversion disorder.” Brain 132(Pt 10): 2889-96. Lesley, A. A. and L. W. Robert (2010). “Cognitive Behavioral Therapy for Somatoform Disorders.” The Psychiatric clinics of North America 33(3): 579-593. Poole, N. A., A. Wuerz, et al. (2010). “Abreaction for conversion disorder: systematic review with meta-analysis.” The British Journal of Psychiatry 197(2): 91-95. Vuilleumier, P. and L. Steven (2005). Hysterical conversion and brain function. Progress in Brain Research, Elsevier. Volume 150: 309-329.

James Amos is the editor of Psychosomatic Medicine, published by Cambridge University Press

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