Conversion disorders are defined as neurological symptoms arising without organic damage to the nervous system, presumably in relation to various emotional stress factors, but the exact neural substrates of these symptoms and the mechanisms responsible for their production remain poorly understood. In the past 15 years, novel insights have been gained with the advent of functional neuroimaging studies in patients suffering from conversion disorders in both motor and non-motor (e.g. somatosensory, visual) domains. Several studies have also compared brain activation patterns in conversion to those observed during hypnosis, where similar functional losses can be evoked by suggestion. The current review summarizes these recent results and the main neurobiological hypotheses proposed to account for conversion symptoms, in particular motor deficits. An emerging model points to an important role of ventromedial prefrontal cortex (VMPFC), precuneus, and perhaps other limbic structures (including amygdala), all frequently found to be hyperactivated in conversion disorders in parallel to impaired recruitment of primary motor and/or sensory pathways at the cortical or subcortical (basal ganglia) level. These findings are only partly shared with hypnosis, where increases in precuneus predominate, together with activation of attentional control systems, but without any activation of VMPFC. Both VMPFC and precuneus are key regions for access to internal representations about the self, integrating information from memory and imagery with affective relevance (in VMPFC) and sensory or agency representations (in precuneus). It is therefore postulated that conversion deficits might result from an alteration of conscious sensorimotor functions and self-awareness under the influence of affective and sensory representations generated in these regions, which might promote certain patterns of behaviors in response to self-relevant emotional states.