Brain, Vol. 124, No. 6, 1077-1090,
June 2001
© 2001 Oxford University Press
Functional neuroanatomical correlates of hysterical sensorimotor loss
1 Departments of Neurology and 2 Nuclear Medicine and Radiology, University Hospital of Geneva, 3 Institute of Psychology, University of Lausanne, Switzerland and 4 Institute of Cognitive Neuroscience, University College London, UK
Correspondence to:
Dr P. Vuilleumier, MD, Institute of Cognitive Neuroscience, University College London, Alexandra House, 17 Queen Square, London WC1N 3AR, UK E-mail: p.vuilleumier{at}ucl.ac.uk
Hysterical conversion disorders refer to functional neurological deficits such as paralysis, anaesthesia or blindness not caused by organic damage but associated with emotional `psychogenic' disturbances. Symptoms are not intentionally feigned by the patients whose handicap often outweighs possible short-term gains. Neural concomitants of their altered experience of sensation and volition are still not known. We assessed brain functional activation in seven patients with unilateral hysterical sensorimotor loss during passive vibratory stimulation of both hands, when their deficit was present and 2–4 months later when they had recovered. Single photon emission computerized tomography using 99mTc-ECD revealed a consistent decrease of regional cerebral blood flow in the thalamus and basal ganglia contralateral to the deficit. Independent parametric mapping and principal component statistical analyses converged to show that such subcortical asymmetries were present in each subject. Importantly, contralateral basal ganglia and thalamic hypoactivation resolved after recovery. Furthermore, lower activation in contralateral caudate during hysterical conversion symptoms predicted poor recovery at follow-up. These results suggest that hysterical conversion deficits may entail a functional disorder in striatothalamocortical circuits controlling sensorimotor function and voluntary motor behaviour. Basal ganglia, especially the caudate nucleus, might be particularly well situated to modulate motor processes based on emotional and situational cues from the limbic system. Remarkably, the same subcortical premotor circuits are also involved in unilateral motor neglect after organic neurological damage, where voluntary limb use may fail despite a lack of true paralysis and intact primary sensorimotor pathways. These findings provide novel constraints for a modern psychobiological theory of hysteria.
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