These data reveal more profound activations of the motor system during AO in conjunction with imagery than during AO alone. These results may have important implications for neurorehabilitation and motor learning.

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Initial historical accounts as well as recent data suggest that emotion processing is dysfunctional in conversion disorder patients and that this alteration may be the pathomechanistic neurocognitive basis for symptoms in conversion disorder. However, to date evidence of direct interaction of altered negative emotion processing with motor control networks in conversion disorder is still lacking. To specifically study the neural correlates of emotion processing interacting with motor networks we used a task combining emotional and sensorimotor stimuli both separately as well as simultaneously during functional magnetic resonance imaging in a well characterized group of 13 conversion disorder patients with functional hemiparesis and 19 demographically matched healthy controls. We performed voxelwise statistical parametrical mapping for a priori regions of interest within emotion processing and motor control networks. Psychophysiological interaction (PPI) was used to test altered functional connectivity of emotion and motor control networks. Only during simultaneous emotional stimulation and passive movement of the affected hand patients displayed left amygdala hyperactivity. PPI revealed increased functional connectivity in patients between the left amygdala and the (pre-)supplemental motor area and the subthalamic nucleus, key regions within the motor control network. These findings suggest a novel mechanistic direct link between dysregulated emotion processing and motor control circuitry in conversion disorder.

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We suggest that the paradoxical decrease of motor excitability during motor imagery is the electrophysiological correlate of a disturbed voluntary control in motor conversion disorder. The results further indicate that this abnormality is not restricted to the clinically affected body part.

The neural mechanisms underlying conversion disorders such as hysterical blindness are at present unknown. Typically, patients are diagnosed through exclusion of neurological disease and the absence of pathologic neurophysiological diagnostic findings. Here, we investigate the neural basis of this disorder by combining electrophysiological (event-related potentials) and hemodynamic measures (functional magnet resonance tomography) in a patient with hysterical blindness before and after successful treatment. Importantly, the blindness was limited to the left upper and right lower visual quadrant offering the possibility to use the other 2 sighted quadrants as controls. While the functional magnetic resonance imaging activations were normal for visual stimulation electrophysiological indices of visual processing were modulated in a specific manner. Before treatment, the amplitude of the N1 event-related potentials component had smaller amplitudes for stimuli presented in the blind quadrants of the visual field. Following successful treatment the N1 component elicited by stimuli presented in formerly blind quadrants had a normal distribution without any amplitude differences between the 4 quadrants. The current findings point out that dissociative disorders such as hysterical blindness may have neurophysiological correlates. Furthermore, the observed neurophysiological pattern suggests an involvement of attentional mechanisms in the neural basis hysterical blindness.

In patients with a functional (psychogenic) paresis, motor conduction tests are, by definition, normal. We investigated whether these patients exhibit an abnormal motor excitability. Four female patients with a functional paresis of the left upper extremity were studied using transcranial magnetic stimulation (TMS). We investigated motor thresholds, intracortical inhibition and intracortical facilitation at rest. Corticospinal excitability was evaluated by single pulse TMS during rest and during imagination of tonic index finger adductions. Data obtained from the affected first dorsal interosseous muscle were compared with the unaffected hand and with a healthy age-matched control group. Three patients demonstrated a flaccid paresis, one patient had a psychogenic dystonia. Motor thresholds, short interval intracortical inhibition and intracortical facilitation recorded from the affected side were normal. In healthy subjects, movement imagination produced an increase of corticospinal excitability. In the patients, motor imagery with the affected index finger resulted in a decrease of corticospinal excitability compared to rest, being significantly different from the unaffected side and from the control group. We suggest that suppression of corticospinal excitability during movement imagination is an electrophysiological correlate of the patients' inability to move voluntarily and provides some insight into the pathophysiology of this disorder.2008 Movement Disorder Society