Abstract:These functional neuroanatomical findings add support to earlier suggestions that manipulation of information is selectively more affected than maintenance of information in persons with schizophrenia. They also suggest the presence of interacting regions of dysfunctional and compensatory prefrontal responses in the dorsolateral and ventrolateral prefrontal cortex, respectively, that are more prominent when information is manipulated. This disrupted prefrontal network is present relatively early in the course … Show more
“…The schizophrenia subjects in previous studies showing VLPFC overactivation also exhibited hypoactivation of DLPFC, leading some investigators to suggest a compensatory role for the VLPFC (Andreasen et al, 1997;Kim et al, 2003;Tan et al, 2005). Our connectivityperformance analysis does not support the idea that increased temporal-VLPFC connectivity is an effective compensatory mechanism, as there was no correlation with performance in either group.…”
Section: Discussioncontrasting
confidence: 86%
“…We are not aware of any studies reporting increased temporal-VLPFC connectivity, although it occurred at subthreshold levels in one study described above (Meyer-Lindenberg et al, 2005, supplementary online data). While both groups in the current study activated VLPFC equally (Ragland et al, 2005), as in Jennings et al (1998) and Barch et al (2001), other studies have found increased task-related activity of VLPFC in schizophrenia (Kim et al, 2003;Bonner-Jackson et al, 2005;Tan et al, 2005). Overactivation of left inferior frontal cortex has also been observed in a resting PET study (Andreasen et al, 1997), and intriguingly, treatment with either haldoperidol or clozapine reduced VLPFC activity (Lahti et al, 2003).…”
Cognitive deficits, including impaired verbal memory, are prominent in schizophrenia and lead to increased disability. Functional neuroimaging of patients with schizophrenia performing memory tasks has revealed abnormal activation patterns in prefrontal cortex and temporo-limbic regions. Aberrant fronto-temporal interactions thus represent a potential pathophysiological mechanism underlying verbal memory deficits, yet this hypothesis of disturbed connectivity is not tested directly with standard activation studies. We performed within-subject correlations of frontal and temporal timeseries to measure functional connectivity during verbal encoding. Our results confirm earlier findings of aberrant fronto-temporal connectivity in schizophrenia, and extend them by identifying distinct alterations within dorsal and ventral prefrontal cortex. Relative to healthy controls, patients with schizophrenia had reduced connectivity between the dorsolateral prefrontal cortex (DLPFC) and temporal lobe areas including parahippocampus and superior temporal gyrus. In contrast, patients showed increased connectivity between a region of ventrolateral prefrontal cortex (VLPFC) and these same temporal lobe regions. Higher temporal-DLPFC connectivity during encoding was associated with better subsequent recognition accuracy in controls, but not patients. Temporal-VLPFC connectivity was uncorrelated with recognition accuracy in either group. The results suggest that reduced temporal-DLPFC connectivity in schizophrenia could underlie encoding deficits, and increased temporal-VLPFC connectivity may represent an ineffective compensatory effort.
“…The schizophrenia subjects in previous studies showing VLPFC overactivation also exhibited hypoactivation of DLPFC, leading some investigators to suggest a compensatory role for the VLPFC (Andreasen et al, 1997;Kim et al, 2003;Tan et al, 2005). Our connectivityperformance analysis does not support the idea that increased temporal-VLPFC connectivity is an effective compensatory mechanism, as there was no correlation with performance in either group.…”
Section: Discussioncontrasting
confidence: 86%
“…We are not aware of any studies reporting increased temporal-VLPFC connectivity, although it occurred at subthreshold levels in one study described above (Meyer-Lindenberg et al, 2005, supplementary online data). While both groups in the current study activated VLPFC equally (Ragland et al, 2005), as in Jennings et al (1998) and Barch et al (2001), other studies have found increased task-related activity of VLPFC in schizophrenia (Kim et al, 2003;Bonner-Jackson et al, 2005;Tan et al, 2005). Overactivation of left inferior frontal cortex has also been observed in a resting PET study (Andreasen et al, 1997), and intriguingly, treatment with either haldoperidol or clozapine reduced VLPFC activity (Lahti et al, 2003).…”
Cognitive deficits, including impaired verbal memory, are prominent in schizophrenia and lead to increased disability. Functional neuroimaging of patients with schizophrenia performing memory tasks has revealed abnormal activation patterns in prefrontal cortex and temporo-limbic regions. Aberrant fronto-temporal interactions thus represent a potential pathophysiological mechanism underlying verbal memory deficits, yet this hypothesis of disturbed connectivity is not tested directly with standard activation studies. We performed within-subject correlations of frontal and temporal timeseries to measure functional connectivity during verbal encoding. Our results confirm earlier findings of aberrant fronto-temporal connectivity in schizophrenia, and extend them by identifying distinct alterations within dorsal and ventral prefrontal cortex. Relative to healthy controls, patients with schizophrenia had reduced connectivity between the dorsolateral prefrontal cortex (DLPFC) and temporal lobe areas including parahippocampus and superior temporal gyrus. In contrast, patients showed increased connectivity between a region of ventrolateral prefrontal cortex (VLPFC) and these same temporal lobe regions. Higher temporal-DLPFC connectivity during encoding was associated with better subsequent recognition accuracy in controls, but not patients. Temporal-VLPFC connectivity was uncorrelated with recognition accuracy in either group. The results suggest that reduced temporal-DLPFC connectivity in schizophrenia could underlie encoding deficits, and increased temporal-VLPFC connectivity may represent an ineffective compensatory effort.
“…Such deficits have been consistently associated with altered lateral prefrontal activity (Tan et al, 2005). In line with these results, recent resting-state fMRI investigations have shown that symptoms of schizophrenia involve widespread hypo-connectivity between frontal areas and temporal, thalamic, and striatal regions Anticevic et al, 2015;Cocchi et al, 2014; van den Heuvel M a n u s c r i p t Sale et al,30 and Fornito, 2014).…”
Please cite this article as: Sale, M.V., Mattingley, J.B., Zalesky, A., Cocchi, L.,Imaging human brain networks to improve the clinical efficacy of noninvasive brain stimulation, Neuroscience and Biobehavioral Reviews (2015), http://dx
“…Repetitive TMS was targeted at the junction of the middle and anterior one-third of the middle frontal gyrus (Talairach coordinates (x, y, z) ÂŒ Ă50, 30, 36), corresponding with the posterior regions of the Brodmann area 9 (BA9), and overlapping with the superior region of BA46 ( Figure 2). The selection of this site was based on a recent meta-analysis of functional imaging studies that examined WM and the activation of the DLPFC (Cannon et al, 2005;Mendrek et al, 2005;Tan et al, 2005).…”
Neuronal oscillations in the gamma (g) frequency range (30-50 Hz) have been associated with cognition. Working memory (WM), a cognitive task involving the on-line maintenance and manipulation of information, elicits increases in g oscillations with greater cognitive demand, particularly in the dorsolateral prefrontal cortex (DLPFC). The generation and modulation of g oscillations have been attributed to inhibitory interneuron networks that use g -aminobutyric acid (GABA) as their principal neurotransmitter. Repetitive transcranial magnetic stimulation (rTMS) represents a non-invasive method to stimulate the cortex that has been shown to modify cognition and GABA inhibitory mechanisms, particularly with higher frequencies (ie, 10-20 Hz). We measured the effect of high-frequency rTMS applied to the DLPFC on g-oscillations elicited during the N-back WM task in healthy individuals. Active rTMS significantly increased g-oscillations generated during the N-back conditions with the greatest cognitive demand. Further, no significant changes were found in other frequency ranges, suggesting that rTMS selectively modulates g-oscillations in the frontal brain regions. These findings provide important insights into the neurophysiological mechanisms that underlie higher-order cognitive processes, and suggest that rTMS may be used as a cognitive enhancing strategy in neuropsychiatric disorders that suffer from cognitive deficits.
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