Hysterical conversion disorders represent "functional" or unexplained neurological deficits such as paralysis or somatosensory losses that are not explained by organic lesions in the nervous system, but arise in the context of "psychogenic" stress or emotional conflicts. After more than a century of both clinical and theoretical interest, the exact nature of such emotional disorders responsible for hysterical symptoms, and their functional consequences on neural systems in the brain, still remain largely unknown. However, several recent studies have used functional brain imaging techniques (such as EEG, fMRI, PET, or SPECT) in the attempt to identify specific neural correlates associated with hysterical conversion symptoms. This article presents a general overview of these findings and of previous neuropsychologically based accounts of hysteria. Functional neuroimaging has revealed selective decreases in the activity of frontal and subcortical circuits involved in motor control during hysterical paralysis, decreases in somatosensory cortices during hysterical anesthesia, or decreases in visual cortex during hysterical blindness. Such changes are usually not accompanied by any significant changes in elementary stages of sensory or motor processing as measured by evoked potentials, although some changes in later stages of integration (such as P300 responses) have been reported. On the other hand, several neuroimaging results have shown increased activation in limbic regions, such as cingulate or orbitofrontal cortex during conversion symptoms affecting different sensory or motor modalities. Taken together, these data generally do not support previous proposals that hysteria might involve an exclusion of sensorimotor representations from awareness through attentional processes. They rather seem to point to a modulation of such representations by primary affective or stress-related factors, perhaps involving primitive reflexive mechanisms of protection and alertness that are partly independent of conscious control, and mediated by dynamic modulatory interactions between limbic and sensorimotor networks. A better understanding of the neuropsychobiological bases of hysterical conversion disorder might therefore be obtained by future imaging studies that compare different conversion symptoms and employ functional connectivity analyses. This should not only lead to improve clinical management of these patients, but also provide new insights on the brain mechanisms of self-awareness.