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Masato Matsuura

Publications and source records attributed to Masato Matsuura.

At least 19 recordsLinked to original sources

Changes in central 5-HT(1A) receptor binding in mesial temporal epilepsy measured by positron emission tomography with [(11)C]WAY100635.

OBJECTIVE: The possible involvement of the brain 5-HT(1A) receptor in epilepsy has been indicated in animal seizure models. Recent in vivo neuroimaging studies demonstrated decreased 5-HT(1A) receptor binding in epilepsy. Using positron emission tomography (PET) with [(11)C]WAY100635, we investigated 5-HT(1A) receptor binding in patients with mesial temporal lobe epilepsy and aimed to clarify the involvement of the brain 5-HT(1A) receptor system in epilepsy. METHOD: PET measurements with [(11)C]WAY100635 were performed on 23 healthy volunteers and 13 patients who were diagnosed with mesial temporal lobe epilepsy based on clinical symptoms and electroencephalogram (EEG) findings. They had non-lesional mesial temporal lobe epilepsy with unilateral EEG foci and no hippocampal atrophy on magnetic resonance imaging. The binding potential (BP) of [(11)C]WAY100635 was calculated by the reference tissue model method. Data were analyzed for each region of interest (ROI) and on a voxel-by-voxel basis by statistical parametric mapping (SPM) system. RESULTS: ROI and voxel-based analyses consistently demonstrated that 5-HT(1A) receptor BP was significantly decreased in the temporal lobe, hippocampus and amygdala on the ipsilateral side of the EEG focus compared to controls. In addition, decreased 5-HT(1A) receptor BP was also observed on the contralateral side of the amygdala. CONCLUSION: 5-HT(1A) receptor binding in patients with mesial temporal lobe epilepsy decreased predominantly in the ipsilateral mesial temporal lobe structures but also in the contralateral side. The imaging of 5-HT(1A) receptor binding by PET detects functional changes of the limbic system in mesial temporal lobe epilepsy, proving to be a sensitive and useful method.

Adult↗

Men and women show distinct brain activations during imagery of sexual and emotional infidelity.

Jealousy-related behaviors such as intimate partner violence and morbid jealousy are more common in males. Principal questionnaire studies suggest that men and women have different modules to process cues of sexual and emotional infidelity. We aimed to elucidate the neural response to sentences depicting sexual and emotional infidelity in men and women using functional magnetic resonance imaging. Although there was no sex difference in the self-rating score of jealousy for sexual and emotional infidelity, men and women showed different brain activation patterns in response to the two types of infidelity. During jealous conditions, men demonstrated greater activation than women in the brain regions involved in sexual/aggressive behaviors such as the amygdala and hypothalamus. In contrast, women demonstrated greater activation in the posterior superior temporal sulcus. Our fMRI results are in favor of the notion that men and women have different neuropsychological modules to process sexual and emotional infidelity. Our findings might contribute to a better understanding of the neural basis of the jealousy-related behaviors predominantly observed in males.

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Language processing and human voice perception in schizophrenia: a functional magnetic resonance imaging study.

BACKGROUND: Neuroimaging studies have demonstrated either reduced left-lateralized activation or reversed language dominance in schizophrenia. These findings of left hemispheric dysfunction could be attributed to language processing tasks, which activate mainly left hemispheric function. Recent functional magnetic resonance imaging studies reported right-lateralized temporal activation by human voice perception, but few studies have investigated activation by human voice in schizophrenia. We aimed to clarify the cerebral function of language processing in schizophrenia patients by considering cerebral activation of human voice perception. METHODS: Fourteen right-handed schizophrenia patients and 14 right-handed controls with matched handedness, sex, and education level were scanned by functional magnetic resonance imaging while listening to sentences (SEN), reverse sentences (rSEN), and identifiable non-vocal sounds (SND). RESULTS: Under the SEN-SND and SEN-rSEN contrasts including language processing, patients showed less activation of the left hemisphere than controls in the language-related fronto-tempo-parietal region, hippocampus, thalamus and cingulate gyrus. Under the rSEN-SND contrast including human voice perception, patients showed less activation than controls in the right-lateralized temporal cortices and bilateral posterior cingulate. CONCLUSIONS: Our results indicate that schizophrenia patients have impairment of broader bilateral cortical-subcortical regions related to both the semantic network in the left hemisphere and the voice-specific network in the right hemisphere.

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Separate processing of different global-motion structures in visual cortex is revealed by FMRI.

The visual system has the remarkable ability to extract several types of meaningful global-motion signals, such as radial motion, translation motion, and rotation, for different visual functions and actions. In the monkey brain, different groups of cells in MST respond best to different types of global motion [1, 2] whereas in lower cortical areas including MT, no such differential responses have been found. Here, we show that an area (or areas) lower than MST in the human brain [3] responds to different types of global motion. A series of human functional magnetic resonance imaging (fMRI) experiments, in which attention was controlled for, indicated that the center of radial motion activates the corresponding location in the V3A representation, whereas translation motion activates mainly in a more peripheral representation of V3A. These results suggest that in the human brain, V3A is an area that differentially responds according to the type of global motion.

Adult↗

Intellectual disability and psychotic disorders of adult epilepsy.

PURPOSE: To investigate the prevalence, psychopathology, and cognitive functions associated with psychotic disorders among adult epilepsy patients with intellectual disability (ID) based on a multicenter study in Japan. METHODS: The study was divided into three phases: a prevalence study of psychotic disorders among new referrals of epilepsy, a polydiagnostic comparative study of patients with psychotic epilepsy and those with schizophrenia, and a neuropsychological study of patients with psychotic epilepsy and education level-matched controls. RESULTS: Among 336 new referrals of epilepsy, a higher prevalence of psychotic disorders was found among patients with ID (24%) than among those with normal intelligence (6%). The psychotic symptoms and operational diagnoses of psychotic epilepsy patients with ID were similar to those of patients with normal intelligence. A wide range (7-86%) of psychotic epilepsy patients was diagnosed as having schizophrenia, depending on the operational criteria used. Patients with psychotic epilepsy had more disturbances in verbal memory and attention functions than controls. CONCLUSIONS: Epilepsy patients with ID show a predisposition to develop psychotic disorders. Distinguishing their psychotic symptoms from those of schizophrenia is difficult. Subtle cognitive disturbances predispose to psychotic disorders in epilepsy.

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A polydiagnostic and dimensional comparison of epileptic psychoses and schizophrenia spectrum disorders.

After establishing the validity of the Japanese version of the Operational Criteria Checklist for Psychotic Illness (OPCRIT), we applied it to 58 consecutive patients with epileptic psychoses (index group) and to age- and sex-matched controls with schizophrenia spectrum disorders (control group). Compared with the control group, the index group had a low family history of schizophrenia, high premorbid personality disorder and unemployment, abrupt or acute onset of psychosis, good recovery with single or multiple episodes, and low deterioration from a premorbid level of function. From 9% to 52% of the index group and 38% to 84% of the control group were diagnosed with schizophrenia according to the operational criteria used. The percentages of patients diagnosed with schizophrenia based on various diagnostic criteria in the two groups were similar. In the index group, a diagnosis of schizophrenia was more commonly made among patients with inter-ictal psychosis than among those with post-ictal psychosis. An exploratory factor analysis identified five factor solutions of manic, negative, depressive, vegetative, and positive symptoms. Although positive and negative factor values were lower in the index group than in the control group, the two groups shared a similar factor profile. These results indicate that the difference in symptomatology between the two groups was quantitative rather than qualitative.

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Functional MRI mapping of brain activation during visually guided saccades and antisaccades: cortical and subcortical networks.

Antisaccade tasks require a subject to inhibit a saccade toward a briefly appearing peripheral target and instead to immediately generate a saccade to an equivalent point in the opposite hemifield. Using functional magnetic resonance imaging (fMRI), we investigated the neural networks required to inhibit reflexive saccades and to voluntarily generate saccades. The results demonstrated that saccade and antisaccade tasks often bilaterally activate frontal, parietal and supplementary eye fields, lenticular nuclei and occipital cortex. Additional activation of bilateral dorsolateral prefrontal cortices, supramarginal gyri, anterior cingulate cortices and thalamus was observed during antisaccade tasks. These results indicate that fronto-parietal and fronto-striato-thalamo-cortical circuits are involved in antisaccade tasks. The fronto-parietal circuit is thought to be related to the planning of saccadic eye movements that involve attentional control, while the fronto-striato-thalamo-cortical circuits connect to cortical region as a feedback network. We speculate that the abnormalities in spatial attention and eye movement control observed in schizophrenia stem from dysfunctions in the fronto-parietal and fronto-striato-thalamo-cortical circuits.

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Mutation screening and association study of the beta-adrenergic receptor kinase 2 gene in schizophrenia families.

Chromosome 22q12 is one of the most promising regions for harboring a risk gene for schizophrenia. We have reported significant linkage of intermediate phenotypes for schizophrenia with markers within or near the beta-adrenergic receptor kinase 2 (ADRBK2, or GRK3) gene, which is highly expressed in dopaminergic pathways in the central nervous system, and mediates homologous desensitization for a variety of neurotransmitters and hormones through phosphorylation of G protein-coupled receptors (GPCRs). A polymorphism in the promoter region of the ADRBK2 was reported to be associated with bipolar disorder. We screened the putative promoter region, and all 21 exonic and flanking intronic regions of the ADRBK2 gene for mutations in 48 schizophrenia probands (including 16 Japanese and 32 Chinese patients), and evaluated the detected polymorphisms and those reported in the JSNP database for associations with schizophrenia in 113 family trios of schizophrenia probands. Four single nucleotide variants in the 5'-UTR/promoter region, and 16 rare variants in exonic and flanking regions, were identified. Among them, the Cys208Ser variant was the only non-synonymous mutation. Cys208Ser was found in one family without cosegregation between the variant and schizophrenia. Moreover, allelic, genotypic and haplotypic analyses provided no evidence for association between alleles at these polymorphisms and schizophrenia. The present study indicates that the ADRBK2 gene is unlikely to contribute strongly to schizophrenia susceptibility in this set of families.

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An fMRI study of differential neural response to affective pictures in schizophrenia.

Although emotional dysfunction is considered a fundamental symptom of schizophrenia, studies investigating the neural basis of emotional dysfunction in schizophrenia are few. Using functional magnetic resonance imaging (fMRI) and a task viewing affective pictures, we aimed to examine automatic emotional response and to elucidate the neural basis of impaired emotional processing in schizophrenia. Fifteen healthy volunteers and 15 schizophrenics were studied. During the scans, the subjects were instructed to indicate how each of the presented pictures made them feel. Whole brain activities in response to the affective pictures were measured by fMRI. Controls recruited the neural circuit including amygdaloid-hippocampal region, prefrontal cortex, thalamus, basal ganglia, cerebellum, midbrain, and visual cortex while viewing unpleasant pictures. Despite an equal behavioral result to controls, the patients showed less activation in the components of the circuit (right amygdala, bilateral hippocampal region, medial prefrontal cortex (MPFC), basal ganglia, thalamus, cerebellum, midbrain, and visual cortex). This study demonstrated functional abnormalities in the neural circuit of emotional processing in schizophrenia. In particular, decreased activation in the right amygdala and MPFC appears to be an important finding related to dysfunctional emotional behavior in schizophrenia.

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Significant linkage to chromosome 22q for exploratory eye movement dysfunction in schizophrenia.

A genome-wide scan for a locus responsible for exploratory eye movement (EEM), which is quantitative and can be disturbed in association with schizophrenia, was performed. A 10-cM resolution genome-wide linkage analysis of the EEM disturbance with 358 highly polymorphic microsatellite markers in 38 nuclear families with 122 members (38 probands, 47 sibs, and 37 parents) including 58 sib-pairs yielded the suggestive linkage to the GCT10C10 marker on chromosome 22q11.2 (LOD = 2.48). Dense mapping with additional markers around the GCT10C10 marker yielded evidence for significant linkage between EEM disturbance and markers D22S429 and D22S310 on chromosome 22q12.1 (LOD score of 4.63) with suggestive evidence for the chromosome region 22q11.2-q12.1. Our findings suggest that a relatively small number of loci may control the schizophrenia-related quantitative EEM trait. We believe that identifying gene(s) on chromosome 22q associated with the EEM phenotype may forward our understanding of the etiology of schizophrenia.

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Family-based association study of the NOTCH4 gene in schizophrenia using Japanese and Chinese samples.

BACKGROUND: A family based association study in a British sample found the NOTCH4 gene to be associated with schizophrenia; however, all six replication studies failed to confirm the finding. METHODS: We performed a family based association study of NOTCH4 and schizophrenia in 123 trios (16 Japanese and 107 Chinese). In addition to the original study's polymorphisms, we examined four new single nucleotide polymorphisms (SNPs)--SNPs_A, B, C and D--around SNP1 of the original study. We genotyped all samples for SNPs_A-D and for SNP1 and (CTG)n of the original study. RESULTS: We found no significant associations between NOTCH4 and schizophrenia or its subtypes for all polymorphisms, regardless of gender. The finding remained negative when the Chinese sample was analyzed separately. Exploratory analyses suggested that SNP_A may be associated with early-onset schizophrenia and that SNP1 may be associated with schizophrenia characterized by numerous negative symptoms. CONCLUSIONS: NOTCH4 is not a significant susceptibility gene for schizophrenia when clinical heterogeneity is ignored; however, NOTCH4 may be associated with early-onset schizophrenia or schizophrenia with many negative symptoms, but these findings should be interpreted cautiously.

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Family-based association study of markers on chromosome 22 in schizophrenia using African-American, European-American, and Chinese families.

Several studies suggest that loci at chromosome 22q11.2-q13 might be linked to susceptibility to schizophrenia. Here we performed family-based association studies on chromosome 22q using 12 DNA microsatellite markers in African-American, European-American, and Chinese pedigrees. The marker D22S683 showed significant linkage and association with schizophrenia in not only the European-American sample but also in a combined sample (European-American and Chinese samples). Notably, D22S683 is located nearby and between D22S278 and D22S283, which have shown linkage and association to schizophrenia in prior reports. However, we found no significant association for the African-American sample. In conclusion, our data provide further support for the idea that the region around D22S683 contains a susceptibility gene for schizophrenia.

Adult↗

Long-, intermediate- and short-acting benzodiazepine effects on human sleep EEG spectra.

The effects of 10 mg haloxazolam (HAX), 4 mg flunitrazepam (FNZ), and 0.5 mg triazolam (TRI), each administered for seven consecutive nights were studied in the sleep electroencephalograms (EEG) of 17 (six HAX, five FNZ and six TRI) healthy male student volunteers. Recordings of C3-A1 EEG data from one baseline night, three drug nights (first, fourth and seventh) and two withdrawal nights (second and fourth) were analyzed using a fast Fourier transformation method. All three drugs induced similar changes in the 0.5 Hz to 40 Hz power spectrum; namely (i) higher frequency (including the sigma and beta bands) activity increased and lower frequency activity reduced on the drug nights; (ii) the enhancement of sigma activity peaked during non-rapid eye movement sleep following the first administration and was maintained at high levels on all drug nights; (iii) beta activity increased through the night after administration of HAX and FNZ, but not TRI, which suggests a blood concentration level dependent increase of beta activity; and (iv) only HAX showed a residual effect on the fourth withdrawal night. These results indicate that (i) chronic administration of these three benzodiazepine derivatives produce similar profiles in sleep EEG spectral changes, with some differences depending on their half-lives and doses; (ii) the mechanism of sigma enhancement is sensitive to even the initial administration night of BDZ; and (iii) frequencies below and above the sigma band are less sensitive to BDZ and also show an increase through the night after administration, suggesting differences in the mechanisms reflected by these EEG frequency bands.

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Multi-center study on post-ictal headache in patients with localization-related epilepsy.

The nature of post-ictal headache (PIH) remains unclear. A multicenter study was conducted in order to evaluate frequency and risk factors for PIH. The subjects consisted of 97 patients with temporal lobe epilepsy (TLE), 65 patients with frontal lobe epilepsy (FLE) and 37 patients with occipital lobe epilepsy (OLE). The subjects were asked about PIH at each institute. Clinical factors of epilepsy were reviewed for each patient and correlated with PIH. Post-ictal headache occurred in 41% of TLE patients, 40% of FLE patients and 59% of OLE patients. Logistic regression analysis revealed that the risk of PIH was significantly higher in OLE than in FLE. In contrast, there were no significant differences in the incidence of PIH between TLE and either OLE or FLE patients. Post-ictal headache occurred significantly more frequently in subjects with generalized tonic-clonic seizure (GTCS) than in those without GTCS. Other clinical factors, such as sex, age, age at onset, duration of illness, seizure frequency, family history of headache and interictal headache were found to have no associations with PIH. A difference was found in the incidence of PIH depending on classification of epilepsy, but only to a relatively slight extent. It was also found that GTCS was significantly related to PIH. These results suggest that both the location of epileptogenic focus and the involvement of certain cerebral areas in the spread of seizure discharges may be closely related to PIH.

Adult↗

Determining vulnerability to schizophrenia in methamphetamine psychosis using exploratory eye movements.

Patients with methamphetamine (MAP) psychosis whose psychotic symptoms continued after MAP withdrawal were observed at Saitama Prefecture Government Psychiatric Hospital. The purpose of the present study was to ascertain whether some of these MAP psychosis subjects have a vulnerability to schizophrenia. Forty-eight patients with MAP psychosis were divided into three groups based on clinical course: transient type, prolonged type and persistent type. Furthermore, the patients with the persistent type were divided into two groups: one group were moderately disturbed in social adaptive functioning and had Global Assessment Functioning scale (GAF) points >50, and the other group consisted of those who were severely disturbed in social adaptive functioning and who had GAF points of < or =50. These MAP patients were tested for exploratory eye movements, which are the vulnerability marker of schizophrenia, and were compared with 30 patients with schizophrenia and 30 healthy control subjects. The responsive search score of the severely disturbed group of patients of the persistent type was lowest, significantly lower than those of the transient type and the healthy controls. It did not differ from that of the schizophrenic subjects. These results suggest that the severely disturbed group of patients with the persistent type of MAP psychosis have a vulnerability to schizophrenia.

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