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Hunter 2 , Mingxiong Huang 3 , Jose M. Canive 2 , and Gregory A. ...doi:10.1093/schbul/sbx023.075 fatcat:aw3s72vnwjeyhce2n4lsnnynje
A large and growing literature has demonstrated a deficit in auditory gating in patients with schizophrenia. Although that deficit has been interpreted as a general gating problem, no deficit has been shown in other sensory modalities. Recent research in our laboratory has examined sensory gating effects in the somatosensory system showing no difference in gating of the primary somatosensory response between patients with schizophrenia and control subjects. This is consistent with recentdoi:10.1016/j.psychres.2006.10.011 pmid:17412427 pmcid:PMC2877382 fatcat:jwsu5rkcmnefrimelsodxvj26a
more »... ral studies showing no cortical structural abnormality in primary somatosensory area in schizophrenia. However, a significant decrease in cortical thickness and gray matter volume loss in secondary somatosensory cortex has recently been reported, suggesting this as a focus for impaired somatosensory gating. Thus, the current study was designed (1) to replicate previous work showing a lack of schizophrenia deficit in primary somatosensory cortex (SI) gating, and (2) to investigate a possible deficit in secondary somatosensory cortex (SII) gating. In a paired-pulse paradigm, dipolar sources were assessed in SI and SII contralateral to unilateral median nerve stimulation. Patients demonstrated no impairment in SI gating, but a robust gating deficit in SII, supporting the presence of cross modal gating deficits in schizophrenia.
Considerable evidence indicates early auditory stimulus processing abnormalities in schizophrenia, but the mechanisms are unclear. The present study examined oscillatory phenomena during a pairedclick paradigm in the superior temporal gyrus (STG) as a possible core problem. The primary question addressed is whether first click and/or second click group differences in the time-domain evoked response in patients with schizophrenia are due to (1) group differences in the magnitude of poststimulusdoi:10.1111/j.1469-8986.2008.00682.x pmid:18665866 pmcid:PMC2685182 fatcat:na4m2fzypjbt7jyp7xtuslfaju
more »... scillatory activity, (2) group differences in poststimulus phase-locking, and/or (3) group differences in the magnitude of ongoing background oscillatory activity. Dense-array magnetoencephalography from 45 controls and 45 patients with schizophrenia produced left-and right-hemisphere STG 50-and 100-ms time-frequency evoked, phase-locking, and total power measures. Whereas first click 100-ms evoked theta and alpha abnormalities were observed bilaterally, evoked low beta-band differences were specific to the left hemisphere. Compared to controls, patients with schizophrenia showed more low-frequency phase variability, and the decreased 100-ms S1 evoked response observed in patients was best predicted by the STG phase-locking measure. Address reprint requests to: J.
Canive has been the recipient of research grant support, honoraria, and/or served as a consultant for the following pharmaceutical companies Abbott, AstraZeneca, Bristol-Myers Squib, Eli Lilly, Organon ...pmid:29713096 pmcid:PMC5875362 fatcat:5jrdp4hebvcthi3f55mlrjabii
Department of Radiology, University of California at San Diego, Merit Review Grants from the Department of Veterans Affairs (Huang, Lee, Harrington), and by National Institute of Health Grants R01-MH65304 (Canive ... F 3:29 ffiffiffi ffi m p where m is the number of MEG/EEG sensors. ... The m Â s sensor waveform matrix B = [b(t 1 ), b(t 2 ), . . . , b(t s )] contains MEG data where m is the number of MEG sensors and s is the number of time points, b(t i ) is an m Â 1 vector of the MEG ...doi:10.1016/j.neuroimage.2006.01.029 pmid:16542857 fatcat:v7ginsfzffbxvie7dfnamzujsi
Cañive. None of the authors have commercial interests constituting potential conflict of interest. Information in this article was previously published only where noted. ...doi:10.1017/s1355617709090225 pmid:19203430 pmcid:PMC2878285 fatcat:r2pvpazvvzgihmtn4czy6iwz4m
Human Brain Mapping
The cortical (auditory and prefrontal) and/or subcortical (thalamic and hippocampal) generators of abnormal electrophysiological responses during sensory gating remain actively debated in the schizophrenia literature. Functional magnetic resonance imaging (fMRI) has the spatial resolution for disambiguating deep or simultaneous sources but has been relatively under-utilized to investigate generators of the gating response. Thirty patients with chronic schizophrenia (SP) and 30 matched controlsdoi:10.1002/hbm.22065 pmid:22461278 pmcid:PMC4020570 fatcat:yqew2gltwnbt5nlgvk7dco3dvy
more »... articipated in the current experiment. Hemodynamic response functions (HRF) for single (S1) and pairs (S1 + S2) of identical (IT; "gating-out" redundant information) or non-identical (NT; "gating-in" novel information) tones were generated through deconvolution. Increased or prolonged activation for patients in conjunction with deactivation for controls was observed within auditory cortex, prefrontal cortex and thalamus in response to single tones during the late hemodynamic response, and these group differences were not associated with clinical or cognitive symptomatology. Although patient hyper-activation to paired-tones conditions was present in several ROI, the effects were not statistically significant for either the gating-out or gating-in conditions. Finally, abnormalities in the post-undershoot of the auditory HRF were also observed for both single and paired tones conditions in patients. In conclusion, the amalgamation of the entire electrophysiological response to both S1 and S2 stimuli may limit hemodynamic sensitivity to paired tones during sensory gating, which may be more readily overcome by paradigms that utilize multiple stimuli rather than pairs. Patient hyperactivation following single tones is suggestive of deficits in basic inhibition, neurovascular abnormalities or a combination of both factors.
José M. Cañive, K08 MH085100 to Dr. J. Christopher Edgar), a VA Merit grant (VA Merit CSR&D: IIR-04-212-3 to Dr. José M. ... Cañive), and University of California at San Diego, Merit Review Grant from the Department of Veterans Affairs to Dr. Mingxiong Huang. ... The M × N sensor waveform matrix B(t) = [b(t 1 ), b(t 2 ), …, b(t N )] contains MEG data where m is the number of MEG sensors and s is the number of time points, b(t i ) is an M × 1 vector of the MEG measurements ...doi:10.1016/j.nicl.2013.05.002 pmid:24179821 pmcid:PMC3777790 fatcat:3jpocj7zhrgsxhztwvqn7miw5i
M = 0.97 h, S.D. = 1.54, patients: M = 0.72 h, S.D. = 1.75; F(1,42)= 0.25, p = 0.617). ... =1.0, p=0.326) or parental education (controls: M=13.3 years, S.D. = 3.1; patients: M = 12 years, S.D. = 2.3; F(1,42) = 2.4, p = 0.129). ...doi:10.1016/j.schres.2006.05.021 pmid:16844347 fatcat:v2uxagkokbfedjhpq33ftsgimy
Cañive. ...doi:10.1016/j.schres.2009.08.014 pmid:19775870 pmcid:PMC3534754 fatcat:xufybmikm5e7xh77h45baez27e
Cañive, and grants from the Mental Illness and Neuroscience Discovery (MIND) Institute to Drs. Thoma and Cañive. ... ) and schizophrenia (M = 14.21 nAm, SD = 6.69) groups, whereas controls' S2 (M = 6.54 nAm, SD = 4.40) was smaller than patients' S2 (M = 9.52, SD = 8.22). ... The schizophrenia group (M = .56, SD = .36) was found to have larger P50 sensory gating ratio than the control group (M = .34, SD = .18), t(42) = 2.351, p = .024. ...doi:10.1111/j.1469-8986.2008.00692.x pmid:18823427 pmcid:PMC2789296 fatcat:65vle56r7nhpzbvukwz3uvxwfe
José M. Cañive, K08 MH085100 to Dr. J. Christopher Edgar), a VA Merit grant (VA Merit CSR&D: IIR-04-212-3 to Dr. José M. ... Cañive), and the University of California at San Diego Merit Review Grant from the Department of Veterans Affairs to Dr. Mingxiong Huang. ... In 4 HC and 5 SZ the left STG 40 Hz response was not well localized (source strength less than 5 nA-m, or location N 15 mm from Heschl's Gyrus). In 1 SZ the right STG 40 Hz was not well localized. ...doi:10.1016/j.nicl.2013.11.004 pmid:24371794 pmcid:PMC3871288 fatcat:755gztbfd5denn35r5agg4bpay
Examination of intrinsic functional connectivity using functional MRI (fMRI) has provided important findings regarding dysconnectivity in schizophrenia. Extending these results using a complementary neuroimaging modality, magnetoencephalography (MEG), we present the first direct comparison of functional connectivity between schizophrenia patients and controls, using these two modalities combined. We developed a novel MEG approach for estimation of networks using MEG that incorporates spatialdoi:10.1016/j.neuroimage.2016.10.011 pmid:27725313 pmcid:PMC5179295 fatcat:i64ogjaegrfjbogvomt33ck7km
more »... ependent component analysis (ICA) and pairwise correlations between independent component timecourses, to estimate intra-and intern-network connectivity. This analysis enables group-level inference and testing of between-group differences. Resting state MEG and fMRI data were acquired from a large sample of healthy controls (n=45) and schizophrenia patients (n=46). Group spatial ICA was performed on fMRI and MEG data to extract intrinsic fMRI and MEG networks and to compensate for signal leakage in MEG. Similar, but not identical spatial independent components were detected for MEG and fMRI. Analysis of functional network connectivity (FNC; i.e., pairwise correlations in network (ICA component) timecourses) revealed a differential between-modalities pattern, with greater connectivity among occipital networks in fMRI and among frontal networks in MEG. Most importantly, significant differences between controls and patients were observed in both modalities. MEG FNC results in particular indicated dysfunctional hyperconnectivity within frontal and temporal networks in patients, while in fMRI FNC was always greater for controls than for patients. This is the first study to apply group spatial ICA as an approach to leakage correction, and as such our results may be biased by spatial leakage effects. Results suggest that combining these two neuroimaging modalities reveals additional disease-relevant patterns of connectivity that were not detectable with fMRI or MEG alone.
The proton magnetic resonance spectroscopy ( 1 H-MRS) signals from glutamate (or the combined glutamate and glutamine signal-Glx) have been found to be greater in various brain regions in people with schizophrenia. Recently, the Psychiatric Genetics Consortium reported that several common single-nucleotide polymorphisms (SNPs) in glutamate-related genes confer increased risk of schizophrenia. Here, we examined the relationship between presence of these risk polymorphisms and brain Glx levels indoi:10.3389/fpsyt.2017.00079 pmid:28659829 pmcid:PMC5466972 fatcat:i57tsfkflzd6hgeuq5lzkt6igu
more »... schizophrenia. Methods: 1 H-MRS imaging data from an axial, supraventricular tissue slab were acquired in 56 schizophrenia patients and 67 healthy subjects. Glx was measured in gray matter (GM) and white matter (WM) regions. The genetic data included six polymorphisms genotyped across an Illumina 5M SNP array. Only three of six glutamate as well as calcium-related SNPs were available for examination. These included three glutamate-related polymorphisms (rs10520163 in CLCN3, rs12704290 in GRM3, and rs12325245 in SLC38A7), and three calcium signaling polymorphisms (rs1339227 in RIMS1, rs7893279 in CACNB2, and rs2007044 in CACNA1C). Summary risk scores for the three glutamate and the three calcium polymorphisms were calculated. results: Glx levels in GM positively correlated with glutamate-related genetic risk score but only in younger (≤36 years) schizophrenia patients (p = 0.01). Glx levels did not correlate with calcium risk scores. Glx was higher in the schizophrenia group compared to levels in controls in GM and WM regardless of age (p < 0.001). conclusion: Elevations in brain Glx are in part, related to common allelic variants of glutamate-related genes known to increase the risk for schizophrenia. Since the glutamate risk scores did not differ between groups, some other genetic or environmental factors likely interact with the variability in glutamate-related risk SNPs to contribute to an increase in brain Glx early in the illness.
Human Brain Mapping
Note: Side refers to the hemisphere showing activation where M = Midline; L = left, and R = right hemisphere. ... Region Side BAs X Y Z Volume (ml) Frontal Lobe Anterior midline M 8/9/10/11/6/24/32 −3 39 21 65.880 Inferior frontal gyrus L 47 −34 30 −11 1.566 Temporal Lobe ...doi:10.1002/hbm.20876 pmid:19777578 pmcid:PMC2826505 fatcat:2kueaje2fvafng7mbp25rbpqcm
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