Long-lasting diagonistic dyspraxia suppressed by rTMS applied to the right motor cortex.

We describe the case of a 58-year-old patient with complete callosal agenesis, who developed after a stroke a long lasting and distressing diagonistic dyspraxia. We found two original treatments to relieve the patient from his left limb conflicting movements. Reinforcing left arm sensory input minimized dyspraxic movements but was difficult to apply daily and was found unsatisfactory by the patient. As left anarchic, unwished movements of diagonistic dyspraxia have been attributed to the lack of inhibition exerted by supplementary motor area on right motor cortex, we applied sham-controlled rTMS to the right motor cortex. This procedure provided a dramatic suppression of left-hand involuntary movements. To our knowledge, this is the first description of the successful treatment of diagonistic dyspraxia.

Caudate nucleus and social cognition: neuropsychological and SPECT evidence from a patient with focal caudate lesion.

Most studies in social cognition have focused on developmental diseases or analyzed the consequences of acquired frontal lesions on the integrity of Theory of Mind (ToM), but, to our knowledge, none to date has addressed the eventual consequences of damage to the basal ganglia on ToM. To investigate the possible consequences of such lesions on social cognition, we tested a selected patient, MVG, a 44-year-old man with a focal caudate nucleus (CN) lesion following stroke. In the aftermath of this stroke, MVG shows loss of empathy and difficulties recognizing emotions in others. The dual aims of this study were first, to evaluate the implications of CN on ToM and recognition of emotion, and second, to discuss these results as a consequence of a disconnection of the sub-cortical orbito-frontal (OF) loop due to caudate damage. We performed a complete neuropsychological assessment of MVG, as well as different tasks evaluating social cognition, such as the Faux-Pas Test and the Reading the Eyes in the Mind Test. No deficits were found in the neuropsychological tests. However, on tasks assessing social cognition, MVG showed impairments in the "warm" or "affective" part of ToM as well as in the ability to recognize negative emotions (i.e., sadness and fear). These results indicate that damage to the head of the left CN can lead to impairment of ToM and emotion recognition. Furthermore, the data shows that, in MVG, such impairment appears to be due to a disconnection of the sub-cortical OF circuit resulting from damage to the CN. Neuro-imaging data tends to confirm this hypothesis by bringing out a hypo-perfusion in both, the territory of his left CN and prefrontal (i.e., ventromedial) brain areas.

The behavioral effects of enriched housing are not altered by serotonin depletion but enrichment alters hippocampal neurochemistry.

To assess a possible role for serotonin in the mediation of the behavioral changes induced by enriched housing conditions (EC), adult female Long-Evans rats sustaining a serotonin depletion (150 microg of 5,7-dihydroxytryptamine, icv) and sham-operated rats were housed postoperatively for 30 days in enriched (12 rats/large cage containing various objects) or standard housing conditions (2 rats/standard laboratory cage). Thereafter, anxiety responses (elevated plus-maze), locomotor activity (in the home-cage), sensori-motor capabilities (beam-walking task), and spatial memory (eight-arm radial maze) were assessed. Monoamine levels were subsequently measured in the frontoparietal cortex and the hippocampus. Overall, EC reduced anxiety-related responses, enhanced sensori-motor performance and improved the memory span in the initial stage of the spatial memory task. Despite a substantial reduction of serotonergic markers in the hippocampus (82%) and the cortex (74%), these positive effects of EC were not altered by the lesion. EC reduced the serotonin levels in the ventral hippocampus (particularly in unlesioned rats: -23%), increased serotonin turnover in the entire hippocampus (particularly in lesioned rats: +36%) and augmented the norepinephrine levels in the dorsal hippocampus (+68% in unlesioned and +49% in lesioned rats); no such alterations were found in the frontoparietal cortex. Our data suggest that an intact serotonergic system is not a prerequisite for the induction of positive behavioral effects by EC. The neurochemical changes found in the hippocampus of EC rats, however, show that the monoaminergic innervation of the hippocampus is a target of EC.