Harvey et al Neurophysiological studies In 1972, Ludwig proposed a model of conversion disorders in which symptoms result from a dysfunction of attention due to increased corticofugal inhibition of afferent stimulation (Ludwig 1972). Such a theory was supported by early findings of reduced somatosensory-evoked responses from the affected compared with the normal leg in a patient with hysterical hemianesthesia (Hernandez-Peon et al 1963). However, this finding was not reliably reproduced and normal evoked potentials are now thought to be a hallmark of conversion disorder (Sierra and Berrios 1999). Research using magnetoencephalography (MEG) has found that patients with psychogenic sensory loss also have normal evoked activity in the secondary somatosensory cortex (Hoechstetter et al 2002). Current understanding of how somatosensory processing mediates conscious sensory experience is limited. Both the primary and secondary somatosensory cortices have been suggested to be of particular importance (Johansen-Berg et al 2000; Schwartz et al 2005), but these findings suggest that any altered processing in patients with conversion symptoms must occur further downstream. More recently studies have focused on the P300 component of event-related response (Picton 1992). Lorenz and colleagues designed a paradigm in which patients were asked to verbally report the awareness of electrical stimuli being applied to their hands during EEG recording (Lorenz et al 1998). When healthy patients were asked to feign lack of awareness of the stimulus on one side, a P300 component of the event-related potential was seen. This was thought to represent the processing of the stimulus and the active withholding of a response. When the same paradigm was used in a patient with sensory loss due to conversion disorder no P300 response to stimulation of the affected limb was seen. This provides the first evidence that conversion disorder is neurophysiologically distinct from feigning, but the evidence awaits replication. Interestingly, a lengthening of latency and a decrease in amplitude of P300 waves has also been described in patients with visual neglect due to parietal lobe lesions (Lhermitte et al 1985). This lends some support to the analogy between symptoms seen in right parietal lesions and those in conversion disorder. Functional neuroimaging The emergence of functional neuroimaging has provided new methods with which to test hypotheses about the neural circuits underlying conversion symptoms (see Table 2). 16 However, the heterogeneous nature of symptoms seen in conversion disorder and the varying methodologies used makes comparison between studies difficult. In 1995 the first reported functional imaging study was conducted on a female nurse who had developed left-sided hysterical paralysis and paresthesia (Tiihonen et al 1995). Single-photon emission computed tomography (SPECT) studies were conducted while her left median nerve was stimulated, both while she was symptomatic and when she had recovered (6 weeks later). There was increased perfusion in the right frontal lobe, and hypoperfusion in the right parietal region when her symptoms were present (Tiihonen et al 1995). Similar results were obtained when Marshall and colleagues performed positron emission tomography (PET) on a female patient with a left-sided paralysis that met the criteria for conversion disorder (Marshall et al 1997). Regional cerebral blood flow was compared between episodes of rest, preparing to move, and attempting to move both her unaffected and affected leg. When preparing to move her affected left leg, there was activation of the left lateral premotor cortex and both cerebeller hemispheres relative to the resting condition, suggesting a readiness to move. However, when this patient attempted to move her affected leg, the right premotor and primary sensori-motor cortex failed to activate normally, but there was increased activation in the right anterior cingulate and right orbitofrontal cortex. It was hypothesized that inhibitory pathways involving the orbitofrontal cortex and anterior cingulate may “disconnect” the premotor areas from the primary motor cortex, preventing the patient’s conscious intention from being translated into action. The authors suggest that the activation seen when this patient was preparing to move her affected limb provides evidence against feigning. However, they do not address the issue of whether preparing to move can itself be feigned. More recently, attempts have been made to replicate these case study findings in larger groups of patients. Yazici and Kostakoglu used SPECT to measure resting cerebral blood flow in five patients with astasia–abasia. They found that four of these five patients had decreased perfusion in their left temporal areas and one patient had decreased perfusion in their left parietal lobe compared with the right side (Yazici and Kostakoglu 1998). However, significant methodological issues question the validity of these findings. Most importantly, the contralateral hemisphere does not provide an adequate control condition, particularly as patients’ symptoms were bilateral. In addition, the patients studied had heterogeneous symptoms and many had Neuropsychiatric Disease and Treatment 2006:2(1)