Harvey et al compared with perceived stimuli applied to the unaffected limb. Unperceived stimuli failed to activate the anterior insula, thalamus, anterior cingulate cortex, and ventrolateral prefrontal cortex, but caused increased activation in the rostral anterior cingulate cortex. Unperceived stimuli also caused deactivation in primary and secondary somato- sensory areas, posterior parietal, and prefrontal cortex. However, the generalizability of these findings is limited by the prominence of chronic pain in these patients, and the interpretation of deactivation seen on fMRI remains controversial (Hutchinson et al 1999). Another fMRI study compared five patients with medically unexplained visual loss meeting criteria for conversion disorder with normal controls (Werring et al 2004). During visual stimulation, these patients had reduced activation in their visual cortex and increased activation in their left inferior frontal cortex, left insula, left corpus striatum, bilateral thalami, limbic structures, midbrain, and the left posterior cingulate cortex. The authors note that the networks activated in these patients are similar to those that are activated in blindsight and suggest this may imply a shift towards implicit visual processing in hysterical blindness (Werring et al 2004). Alternatively, they speculate that this activation may represent complex visual processing resulting in inhibition of primary visual areas. It is, however, difficult to interpret this apparent left-sided activation given that patients with both left-sided and right-sided visual deficits were included in this study. The findings of all of these functional imaging studies are summarized in Table 2. Conversion disorder versus feigning Functional imaging has also been used to compare those with conversion disorder with others who have been instructed to feign their symptoms. Spence et al used PET to compare three patients with weakness due to a conversion syndrome with both normal controls and controls instructed to feign weakness (Spence et al 2000). During a simple motor task, those with conversion syndrome had hypo- activation of their left dorsolateral prefrontal cortex (LDLPFC) compared with both normal controls and feigners (Spence et al 2000). This would be consistent with the known role of the dorsolateral prefrontal cortex in volition and willed action (Frith et al 1991; Jahanshahi et al 1995). However, while the patients in this study were euthymic, they all had a past history of depression, which has been 18 suggested as an alternative explanation for the left frontal hypo-activity seen (Vuilleumier et al 2001). An alternative, novel approach in this field has been the use of hypnosis as a model for conversion disorders. Hypnosis can produce a compelling experience of subjective paralysis and thus may have some conceptual links with conversion disorder. In order to establish hypnotically induced paralysis as a model for conversion disorder, Halligan and colleagues replicated the methods used in an earlier imaging study of a patient with conversion disorder and demonstrated that a subject with hypnotic paralysis activated similar brain areas when they tried to move the affected limb as those seen in conversion disorder (Halligan, Athwal, et al 2000). Based on these results Ward et al (2003) conducted a study using 12 healthy volunteers who each had 2 different paralysis conditions created under hypnosis: a subjectively experienced paralysis, and a condition where subjects were aware there was no paralysis but were instructed to feign weakness. PET scanning measured regional cerebral blood flow at rest and on attempting to move the affected left leg. Using Statistical Parametric Mapping analysis there was no significant difference in activation during attempts to move between the two paralysis conditions (Ward et al 2003). However, a small volume correction analysis based around a region of interest from a previous study (Spence et al 2000) did find increased activation in the left ventrolateral prefrontal cortex (LVLPFC) during feigning compared with subjectively experienced paralysis (Ward et al 2003). The authors argue that this is broadly consistent with the finding of Spence et al (2000) of activation of the LDLFC during feigning, not only because of the proximity of these regions, but also because Spence et al reported a separate peak of significant activation in the LVLPFC. The LVLPFC may therefore have a role in the conscious volitional inhibition seen in feigning (Ward et al 2003). This would be consistent with functional imaging studies of deception, which have found lying to be associated with increased activity in the VLPFC (Spence et al 2001). It should, however, be noted that the effect seen in the Ward et al study was small and only significant in one of the two methods of analysis used. While the hypnosis paradigm avoids many of the confounders and co- morbidities that have limited other studies, it remains uncertain how far these results can be generalized. The neurobiological processes involved in such short-lived, experimental conditions may be very different to those involved in the more chronic and complex cases seen in clinical practice (Ward et al 2003). Neuropsychiatric Disease and Treatment 2006:2(1)