Keita Ueda

Abnormal asymmetry of white matter integrity in schizophrenia revealed by voxelwise diffusion tensor imaging.

A number of magnetic resonance imaging (MRI) studies have revealed morphological cortical asymmetry in the normal human brain, and reduction or inversion of such hemispheric asymmetry has been reported in schizophrenia. On the other hand, diffusion tensor imaging (DTI) studies have reported inconsistent findings concerning abnormal asymmetry of white matter integrity in schizophrenia. Our aim was to confirm whether there is reduced or inverted asymmetry of white matter integrity in the whole brain in schizophrenia. For this study, 26 right‐handed schizophrenia patients, and 32 matched healthy control subjects were investigated. Voxelwise analysis of DTI data was performed using the tract‐based spatial statistics. The fractional anisotropy (FA) images were normalized and projected onto the symmetrical white matter skeleton, and the laterality index (LI) of FA, determined by 2 × (left ‐ right)/(left + right), was calculated. The results reveal that schizophrenia patients and healthy controls showed similar patterns of overall FA asymmetries. In the group comparison, patients showed significant reduction of LI in the external capsule (EC), and posterior limb of the internal capsule (PLIC). The EC cluster revealed increased rightward asymmetry, and the PLIC cluster showed reduced leftward asymmetry. Rightward‐shift of FA in the EC cluster correlated with negative symptom severity. Considering that the EC cluster includes the uncinate and inferior occipitofrontal fasciculi, which have connections to the orbitofrontal cortex, abnormal asymmetry of white matter integrity in schizophrenia may play a crucial role in the pathogenesis of schizophrenia, through the altered connectivity to the orbitofrontal cortex. Hum Brain Mapp, 2011.

Liberal bias mediates emotion recognition deficits in frontal traumatic brain injury

It is well-known that patients having sustained frontal-lobe traumatic brain injury (TBI) are severely impaired on tests of emotion recognition. Indeed, these patients have significant difficulty recognizing facial expressions of emotion, and such deficits are often associated with decreased social functioning and poor quality of life. As of yet, no studies have examined the response patterns which underlie facial emotion recognition impairment in TBI and which may lend clarity to the interpretation of deficits. Therefore, the present study aimed to characterize response patterns in facial emotion recognition in 14 patients with frontal TBI compared to 22 matched control subjects, using a task which required participants to rate the intensity of each emotion (happiness, sadness, anger, disgust, surprise and fear) of a series of photographs of emotional and neutral faces. Results first confirmed the presence of facial emotion recognition impairment in TBI, and further revealed that patients displayed a liberal bias when rating facial expressions, leading them to associate intense ratings of incorrect emotional labels to sad, disgusted, surprised and fearful facial expressions. These findings are generally in line with prior studies which also report important facial affect recognition deficits in TBI patients, particularly for negative emotions.

Subthalamic nucleus deep brain stimulation restores normal rapid eye movement sleep in Parkinson's disease.

In Parkinsons disease, sleep disturbance is a common occurrence.

Social cognition and its relationship to functional outcomes in patients with sustained acquired brain injury

Deficits in social cognition are common after traumatic brain injury (TBI). However, little is known about how such deficits affect functional outcomes. The purpose of this study was to investigate the relationship between social cognition and functional outcomes in patients with TBI. We studied this relationship in 20 patients with TBI over the course of 1 year post-injury. Patients completed neurocognitive assessments and social cognition tasks. The social cognition tasks included an emotion-perception task and three theory of mind tasks: the Faux Pas test, Reading the Mind in the Eyes (Eyes) test, and the Moving-Shapes paradigm. The Craig Handicap Assessment and Reporting Technique was used to assess functional outcomes. Compared with our database of normal subjects, patients showed impairments in all social cognition tasks. Multiple regression analysis revealed that theory of mind ability as measured by the Eyes test was the best predictor of the cognitive aspects of functional outcomes. The findings of this pilot study suggest that the degree to which a patient can predict what others are thinking is an important measure that can estimate functional outcomes over 1 year following TBI.

Social cognition in schizophrenia: similarities and differences of emotional perception from patients with focal frontal lesions

The structural and functional abnormalities of the frontal lobes, the region implicated in social information processing, have been suspected to underlie social cognitive impairments in schizophrenia. However, multiple structures, including the limbic/paralimbic areas that are also important for social cognition, have been reported to be abnormal in schizophrenia. The aim of this study is to investigate the extent to which the frontal lobe dysfunction accounts for social cognitive impairments in schizophrenia by comparing with patients who have focal frontal lobe injuries. Social cognitive abilities, focusing on affective aspects, were examined by an emotion intensity recognition task, which is sensitive to the amygdala function, and the emotion attribution tasks, which rely mainly on the frontal lobe function. Individuals with schizophrenia were impaired on the emotion intensity recognition task as well as on the emotion attribution tasks as compared with healthy subjects. By contrast, the frontal lobe-damaged group was defective in the emotion attribution tasks but not in the emotion intensity recognition task. Our results indicated that social cognitive impairments observed in schizophrenia can be accounted for partly by their frontal lobe pathology. Other aspects of social cognitive impairments could also be associated with the extra-frontal pathology, such as the amygdala.

Rhodium-catalysed cyclisation reaction of allenynes with arylboronic acids

Allenynes having malonate-based tethers reacted with arylboronic acids in the presence of a rhodium(I) catalyst to sequentially form three carbon-carbon bonds, and arylated bicyclic skeletons were constructed in a stereoselective manner.

Investigating association of brain volumes with intracranial capacity in schizophrenia

Intracranial volume (ICV) is usually treated as a global or nuisance covariate in almost all volumetric studies of schizophrenia. However, validation for this analytic method has seldom been accomplished. In this study, we aimed to determine the effects of ICV on gray matter (GM) and white matter (WM) volumes. Sixty-three patients with schizophrenia and sixty normal controls were recruited; and high resolution T1 weighted images were obtained by 3T-MRI. After segmentation and normalization of the images into GM, WM, and cerebrospinal fluid (CSF), multiple regression analyses of global GM and WM volumes were performed using explanatory variables such as diagnosis, ICV, and diagnosis-ICV interaction. In addition, associations between regional GM and WM volumes with ICV were also investigated using voxel-based morphometry (VBM). No significant interaction between diagnosis and ICV was found for global GM volume, whereas interactions were detected in restricted GM areas using VBM. On the other hand, an interaction between ICV and diagnosis was found in WM not only for regional volumes, but also for global WM volume. The regression slope of global WM volumes against ICV was steeper in patients with schizophrenia than in healthy controls. These results imply that ICV should be carefully evaluated in the analyses of volumetric studies of schizophrenia, especially when analyzing WM volumes.

Corpus Callosum Pathology as a Potential Surrogate Marker of Cognitive Impairment in Diffuse Axonal Injury

Diffuse axonal injury is a major form of traumatic brain injury. Neuropsychological assessments and high-resolution structural MRI were conducted using T1-weighted and diffusion tensor imaging. This study included 10 patients with diffuse axonal injury (all men, mean age 30.8±10.5 years) and 12 age- and sex-matched normal control participants. Patients with diffuse axonal injury had widespread volume reductions and lower fractional anisotropy in the corpus callosum (CC) compared with controls. Furthermore, cognitive processing speed was associated with reductions in white matter volume and fractional anisotropy in the CC. These findings suggest that CC pathology may be a potential surrogate marker of the cognitive deficits in these patients.

Hypothalamic-amygdalar-brainstem volume reduction in a patient with narcolepsy secondary to diffuse axonal injury.

A 17-year-old male with diffuse axonal injury (DAI) was referred to our psychiatric clinic with a diagnosis of depression. However, further investigation indicated that he had narcolepsy without cataplexy secondary to DAI. We assessed regional volume alterations in the patient; MRI analysis showed a significant decrease in the volume of the hypothalamus, left amygdala, and brainstem. Our findings add to further understanding of the structural basis of secondary narcolepsy, and may provide basis for future neuroimaging studies on sleep disturbances in traumatic brain injury (TBI).

Cognitive Function of Patients with Adult Moyamoya Disease

BACKGROUND Neurocognitive impairment is one of several unsolved social issues faced by patients with moyamoya disease. Although efforts have been made to investigate cognitive function using neuropsychologic tasks, generalizability has been limited. Here, in a preliminary study, we used structured neuropsychologic tasks to establish a standardized neuropsychologic assessment for adult moyamoya patients with and without difficulty in social independence. METHODS Ten patients with neuroradiologically confirmed adult moyamoya disease (3 male, 7 female) participated. Half of all subjects did not have difficulty with social independence (group 1) and the others had (group 2). Group differences were evaluated after basic cognitive abilities and frontal lobe function were tested. RESULTS Although the mean age of group 1 was substantially higher than that of group 2, disease duration did not differ significantly between groups. Means scores for intelligence functions including all subtests for basic cognitive abilities were higher in group 1 compared with group 2. Scores from only 2 frontal lobe evaluation tasks (Trail Making Test B and Theory of Mind) were significantly different between groups. CONCLUSIONS This preliminary study provides a profile of neurocognitive dysfunction in adult patients with moyamoya disease using structured neuropsychologic tasks. A broad range of cognitive functions was disrupted particularly in the patients who had difficulty with social independence. To obtain stronger evidence regarding neurocognitive dysfunction in patients with moyamoya disease, a multicenter prospective study is essential.