Understanding Conversion Disorder: Electrophysiological and behavioural evidence for impaired neuromotor preparation and movement execution

Abstract

Conversion Disorder, originally hysteria, affects the voluntary motor system by disrupting the production of normal volitional movement and is characterised by unexplained neurological symptoms without an organic cause; unlike Malingering, where symptoms are intentionally produced or feigned (American Psychiatric Association, 1994). This thesis contains two studies. Study 1 examined two competing hypotheses, that disruption of either motor preparation or execution underlies the movement deficits associated with Conversion Disorder. The effect of movement-related uncertainty on motor preparation and execution was also determined using a precued reaction time (RT) paradigm in which participants made rapid finger flexions to an imperative visual stimulus. A precue provided complete (simple RT) or partial (2-choice RT) information about the response hand (left or right) and/or finger (index or middle). Electroencephalographic, electromyographic and kinematic measures were recorded during motor preparation and execution. In Study 1, movement performance of six individuals with upper limb unilateral conversion paresis was compared to twelve neurologically normal participants. Results indicated that Conversion Disorder patients initiated and executed movement more slowly and generated less force with their affected hand, and were slower overall than controls. Contingent negative variation (CNV) amplitudes were considerably smaller for affected hand responses, indicating impaired preparatory processes, particularly when patients knew in advance they had to prepare to move with their affected hand. Study 2 examined whether feigned paresis demonstrated behavioural and brain activity outcomes similar to conversion paresis. Two groups of twelve neurologically normal individuals were instructed to imagine they had difficulty moving their left upper limb under one of two instruction methods: “Imaginary resistance” or “diminished effort”. The effect of these instructions on motor preparation and execution were investigated using the same methods as in Study 1. The results of Study 2 indicated that participants instructed to feign paresis also initiated and executed movement more slowly and generated less force with their affected hand. CNV amplitudes were not affected by feigning. The nature of the feigning instruction had no effect on motor preparation or execution. Consistent with an integrated model of Conversion Disorder, both the preparation and execution phases of voluntary movement were significantly impaired in conversion and feigned paresis. Conversion paresis appears difficult to dissociate from feigned paresis when examining the behavioural and muscle activity data from the affected hand. However, differences in CNV amplitude between patients and feigning participants demonstrated changes in brain function during movement preparation that is specific to Conversion Disorder. This novel finding supports the use of motor event-related potentials as an additional approach to examine unexplained neurological motor symptoms. The experiments reported in this thesis provide new knowledge about the temporal organisation of brain function, muscle activity and behaviour underlying conversion and feigned symptoms. Future studies could build on these efforts by explaining in greater detail the functional mechanisms acting within motor areas of the brain that disrupt normal motor preparation and execution in Conversion Disorder. Whether the deficits in neuromotor preparation in Conversion Disorder are due to a prefrontal inhibitory mechanism or deficits in volition remain to be determined.