Structural connectivity between the hippocampus and cortical/subcortical area relates to cognitive impairment in schizophrenia but not in mood disorders

Cognitive impairment in schizophrenia and other psychiatric disorders is a challenge to be overcome in order to maintain patients' quality of life and social function. The neurological pathogenesis of cognitive impairment requires further elucidation. In general, the hippocampus interacts between the cortical and subcortical areas for information processing and consolidation and has an important role in memory. We examined the relationship between structural connectivity of the hippocampus and cortical/subcortical areas and cognitive impairment in schizophrenia, major depressive disorder and bipolar disorder. Subjects comprised 21 healthy controls, 19 patients with schizophrenia, 20 patients with bipolar disorder and 18 patients with major depressive disorder. Diffusion-weighted tensor images data were processed using ProbtrackX2 to calculate the structural connectivity between the hippocampus and cortical/subcortical areas. Cognitive function was assessed using the Brief Assessment of Cognition in schizophrenia composite score. Hippocampal structural connectivity index was significantly correlated with composite score in the schizophrenia group but not in the healthy control, major depressive disorder or bipolar disorder groups. There were no statistically significant differences in hippocampal structural connectivity index between the four groups. Structural connectivity between the hippocampus and cortical/subcortical areas is suggested to be a pathophysiological mechanism of comprehensive cognitive impairment in schizophrenia.     

Prismatic displacement of vision induces transient changes in the timing of eye-hand coordination

Eye-hand coordination was investigated during a task of finger pointing toward visual targets viewed through wedge prisms. Hand and eye latencies and movement times were identical during the control condition and at the end of prism exposure. A temporal reorganization of eye and hand movements was observed during the course of adaptation. During the earlier stage of prism exposure, the time gap between the end of the eye saccade and the onset of hand movement was increased from a control time of 23 to 68 msec. This suggests that a time-consuming process occurred during the early prism-exposure period. The evolution of this time gap was correlated with the evolution of pointing errors during the early stage of prism exposure, in such a way that both measures increased at the onset of prism exposure and decreased almost back to control values within about 10 trials. However, spatial error was not entirely corrected, even late in prism exposure when the temporal organization of eye and hand had returned to baseline. These data suggest that two different adaptive mechanisms were at work: a rather short-term mechanism, involved in normal coordination of spatially aligned eye and hand systems, and a long-term mechanism, responsible for remapping spatially misaligned systems. The former mechanism can be strategically employed to quickly optimize accuracy in a situation involving misalignment, but completely adaptive behavior must await the slower-acting latter mechanism to achieve longterm spatial alignment.