Schizophrenic patients present abnormalities in a variety of eye movement tasks. Exploratory eye movement (EEM) dysfunction appears to be particularly specific to schizophrenia. However, the underlying mechanisms of EEM dysfunction in schizophrenia are not clearly understood. To assess the potential neuroanatomical substrates of EEM, we recorded EEM performance and conducted a voxel-based morphometric analysis of gray matter in 33 schizophrenic patients and 29 well matched healthy controls. In schizophrenic patients, decreased responsive search score (RSS) and widespread gray matter density (GMD) reductions were observed. Moreover, the RSS was positively correlated with GMD in distributed brain regions in schizophrenic patients. Furthermore, in schizophrenic patients, some brain regions with neuroanatomical deficits overlapped with some ones associated with RSS. These brain regions constituted an occipito-tempro-frontal circuitry involved in visual information processing and eye movement control, including the left calcarine cortex [Brodmann area (BA) 17], the left cuneus (BA 18), the left superior occipital cortex (BA 18/19), the left superior frontal gyrus (BA 6), the left cerebellum, the right lingual cortex (BA 17/18), the right middle occipital cortex (BA19), the right inferior temporal cortex (BA 37), the right dorsolateral prefrontal cortex (BA 46) and bilateral precentral gyri (BA 6) extending to the frontal eye fields (FEF, BA 8). To our knowledge, we firstly reported empirical evidence that gray matter loss in the occipito-tempro-frontal neuroanatomical circuitry of visual processing system was associated with EEM performance in schizophrenia, which may be helpful for the future effort to reveal the underlying neural mechanisms for EEM disturbances in schizophrenia.
BackgroundShared neuropathological features between schizophrenic patients and their first-degree relatives have potential as indicators of genetic vulnerability to schizophrenia. We sought to explore genetic influences on brain morphology and function in schizophrenic patients and their relatives.MethodsUsing a multimodal imaging strategy, we studied 33 schizophrenic patients, 55 of their unaffected parents, 30 healthy controls for patients, and 29 healthy controls for parents with voxel-based morphometry of structural MRI scans and functional connectivity analysis of resting-state functional MRI data.ResultsSchizophrenic patients showed widespread gray matter reductions in the bilateral frontal cortices, bilateral insulae, bilateral occipital cortices, left amygdala and right thalamus, whereas their parents showed more localized reductions in the left amygdala, left thalamus and right orbitofrontal cortex. Patients and their parents shared gray matter loss in the left amygdala. Further investigation of the resting-state functional connectivity of the amygdala in the patients showed abnormal functional connectivity with the bilateral orbitofrontal cortices, bilateral precunei, bilateral dorsolateral frontal cortices and right insula. Their parents showed slightly less, but similar changes in the pattern in the amygdala connectivity. Co-occurrences of abnormal connectivity of the left amygdala with the left orbitofrontal cortex, right dorsolateral frontal cortex and right precuneus were observed in schizophrenic patients and their parents.ConclusionsOur findings suggest a potential genetic influence on structural and functional abnormalities of the amygdala in schizophrenia. Such information could help future efforts to identify the endophenotypes that characterize the complex disorder of schizophrenia.
The present study aimed to explore the effect of computerized multi-domain cognitive training (MDCT) on brain gray matter volume and neuropsychological performance in patients with amnestic mild cognitive impairment (amnestic MCI). Twenty-one patients with amnestic MCI participated in a computerized MDCT program. The program targeted a broad set of cognitive domains via programs focused on reasoning, memory, visuospatial, language, calculation, and attention. Seventeen Participants completed the intervention and all completed a battery of neuropsychological tests to evaluate cognitive function while 12 out of 17 underwent 3 T MRI scanning before and after the intervention to measure gray matter (GM) volume. We examined correlations between the changes in neuropsychological scores and GM volumes across participants after the intervention. After training, we observed significant increases in GM volume in the right angular gyrus (AG) and other parietal subareas near the intraparietal sulcus (p < 0.05, FWE-corrected, 10000 permutations). However, we found no significant changes in neuropsychological test scores (p > 0.05). A correlation analysis revealed positive correlations between the changes in GM volume in the right AG and scores in the immediate recall component of the Hopkins Verbal Learning Test-Revised (HVLT-R) (r = 0.64, p = 0.024) and the Brief Visuospatial Memory Test–Revised (BVMT-R) (r = 0.67, p = 0.016). Our findings indicate that a computerized MDCT program may protect patients with amnestic MCI against brain GM volume loss and has potential in preserving general cognition. Thus, our non-pharmacological intervention may slow the rate of disease progression.
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