Time-course of motor inhibition during hypnotic paralysis: EEG topographical and source analysis.

Cognitive hypotheses of hypnotic phenomena have proposed that executive attentional systems may be either inhibited or overactivated to produce a selective alteration or disconnection of some mental operations. Recent brain imaging studies have reported changes in activity in both medial (anterior cingulate) and lateral (inferior) prefrontal areas during hypnotically induced paralysis, overlapping with areas associated with attentional control as well as inhibitory processes. To compare motor inhibition mechanisms responsible for paralysis during hypnosis and those recruited by voluntary inhibition, we used electroencephalography (EEG) to record brain activity during a modified bimanual Go-Nogo task, which was performed either in a normal baseline condition or during unilateral paralysis caused by hypnotic suggestion or by simulation (in two groups of participants, each tested once with both hands valid and once with unilateral paralysis). This paradigm allowed us to identify patterns of neural activity specifically associated with hypnotically induced paralysis, relative to voluntary inhibition during simulation or Nogo trials. We used a topographical EEG analysis technique to investigate both the spatial organization and the temporal sequence of neural processes activated in these different conditions, and to localize the underlying anatomical generators through minimum-norm methods. We found that preparatory activations were similar in all conditions, despite left hypnotic paralysis, indicating preserved motor intentions. A large P3-like activity was generated by voluntary inhibition during voluntary inhibition (Nogo), with neural sources in medial prefrontal areas, while hypnotic paralysis was associated with a distinctive topography activity during the same time-range and specific sources in right inferior frontal cortex. These results add support to the view that hypnosis might act by enhancing executive control systems mediated by right prefrontal areas, but does not produce paralysis via direct motor inhibition processes normally used for the voluntary suppression of actions.

Neural bases of hypoactive sexual desire disorder in women: an event-related FMRI study.

INTRODUCTION: Although there is an abundant debate regarding the mechanisms sustaining one of the most common sexual complaints among women, i.e., female hypoactive sexual desire disorder (HSDD), little remains known about the specific neural bases of this disorder. AIM: The main goal of this study was to determine whether women with HSDD showed differential patterns of activation within the brain network that is active for sexual desire in subjects without HSDD. METHODS: A total of 28 right-handed women participated in this study (mean age 31.1±7.02 years). Thirteen out of the 28 women had HSDD (HSDD participants), while 15 women reported no hypoactive sexual desire disorder (NHSDD participants). Using event-related functional magnetic resonance imaging (fMRI), we compared the regional cerebral blood flow responses between these two groups of participants, while they were looking at erotic vs. non-erotic stimuli. MAIN OUTCOME MEASURE: Blood-oxygenation level dependent (BOLD) signal changes in response to erotic stimuli (compared with non-erotic stimuli). Statistical Parametric Mapping was used to identify brain regions that demonstrated significant differential activations between stimuli and between groups. RESULTS: As expected, behavioral results showed that NHSDD participants rated erotic stimuli significantly higher than HSDD participants did on a 10-point desirable scale. No rating difference was observed for the non-erotic stimuli between NHSDD and HSDD participants. Our functional neuroimaging results extended these data by demonstrating two distinct types of neural changes in participants with and without HSDD. In comparison with HSDD participants, participants without HSDD demonstrated more activation in brain areas involved in the processing of erotic stimuli, including intraparietal sulcus, dorsal anterior cingulate gyrus, and ento/perirhinal region. Interestingly, HSDD participants also showed additional activations in brain areas associated with higher order social and cognitive functions, such as inferior parietal lobule, inferior frontal gyrus, and posterior medial occipital gyrus. CONCLUSION: Together, these findings indicate that HSDD participants do not only show a hypo activation in brain areas mediating sexual desire, but also a different brain network of hyper activation, which might reflect differences in subjective, social, and cognitive interpretations of erotic stimuli. Collectively, these data are in line with the incentive motivation model of sexual functioning.

The brain under self-control: modulation of inhibitory and monitoring cortical networks during hypnotic paralysis.

Brain mechanisms of hypnosis are poorly known. Cognitive accounts proposed that executive attentional systems may cause selective inhibition or disconnection of some mental operations. To assess motor and inhibitory brain circuits during hypnotic paralysis, we designed a go-no-go task while volunteers underwent functional magnetic resonance imaging (fMRI) in three conditions: normal state, hypnotic left-hand paralysis, and feigned paralysis. Preparatory activation arose in right motor cortex despite left hypnotic paralysis, indicating preserved motor intentions, but with concomitant increases in precuneus regions that normally mediate imagery and self-awareness. Precuneus also showed enhanced functional connectivity with right motor cortex. Right frontal areas subserving inhibition were activated by no-go trials in normal state and by feigned paralysis, but irrespective of motor blockade or execution during hypnosis. These results suggest that hypnosis may enhance self-monitoring processes to allow internal representations generated by the suggestion to guide behavior but does not act through direct motor inhibition.

Motor inhibition in hysterical conversion paralysis.

Brain mechanisms underlying hysterical conversion symptoms are still poorly known. Recent hypotheses suggested that activation of motor pathways might be suppressed by inhibitory signals based on particular emotional situations. To assess motor and inhibitory brain circuits during conversion paralysis, we designed a go-nogo task while a patient underwent functional magnetic resonance imaging (fMRI). Preparatory activation arose in right motor cortex despite left paralysis, indicating preserved motor intentions, but with concomitant increases in vmPFC regions that normally mediate motivational and affective processing. Failure to execute movement on go trials with the affected left hand was associated with activations in precuneus and ventrolateral frontal gyrus. However, right frontal areas normally subserving inhibition were activated by nogo trials for the right (normal) hand, but not during go trials for the left hand (affected by conversion paralysis). By contrast, a group of healthy controls who were asked to feign paralysis showed similar activation on nogo trials and left-go trials with simulated weakness, suggesting that distinct inhibitory mechanisms are implicated in simulation and conversion paralysis. In the patient, right motor cortex also showed enhanced functional connectivity with the posterior cingulate cortex, precuneus, and vmPFC. These results suggest that conversion symptoms do not act through cognitive inhibitory circuits, but involve selective activations in midline brain regions associated with self-related representations and emotion regulation.