Functional neuroimaging of working memory in schizophrenia: Task performance as a moderating variable.

Snellenberg, Jared X. Van; Torres, Ivan J.; Thornton, Allen E.

doi:10.1037/0894-4105.20.5.497

Cited by 142 publications

(127 citation statements)

References 59 publications

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“…This relationship between performance and activation reached significance in right dlPFC, left vlPFC, and bilateral premotor cortex. Remarkably, the same lateralization pattern was found in a previous study comparing performance subgroups of patients and controls (Tan et al, 2006) and is additionally supported by a meta-analysis indicating a strong performance-activation relationship in right dlPFC (Van Snellenberg et al, 2006). Previous studies indicate that this relationship is mediated by dopamine: while WM capacity correlated positively with dopamine synthesis in healthy subjects (Cools et al, 2008), the latter predicted dlPFC activation during WM in prodromal subjects (Fusar-Poli et al, 2010).…”

Section: Prefrontal Activation and Cognitive Performancesupporting

confidence: 84%

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Reduced Prefrontal-Parietal Effective Connectivity and Working Memory Deficits in Schizophrenia

et al. 2012

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The neural mechanisms behind cognitive deficits in schizophrenia still remain unclear. Functional neuroimaging studies on working memory (WM) yielded inconsistent results, suggesting task performance as a moderating variable of prefrontal activation. Beyond regional specific activation, disordered integration of brain regions was supposed as a critical pathophysiological mechanism of cognitive deficits in schizophrenia. Here, we first hypothesized that prefrontal activation implicated in WM depends primarily on task performance and therefore stratified participants into performance subgroups. Second, in line with the dysconnectivity hypothesis, we asked whether connectivity in the prefrontal-parietal network underlying WM is altered in all patients. We used functional magnetic resonance imaging in human subjects (41 schizophrenia patients, 42 healthy controls) and dynamic causal modeling to examine effective connectivity during a WM task. In line with our first hypothesis, we found that prefrontal activation was differentially modulated by task performance: there was a significant task by group by performance interaction revealing an increase of activation with performance in patients and a decrease with performance in controls. Beyond that, we show for the first time that WM-dependent effective connectivity from prefrontal to parietal cortex is reduced in all schizophrenia patients. This finding was independent of performance. In conclusion, our results are in line with the highly influential hypothesis that the relationship between WM performance and prefrontal activation follows an inverted U-shaped function. Moreover, this study in a large sample of patients reveals a mechanism underlying prefrontal inefficiency and cognitive deficits in schizophrenia, thereby providing direct experimental evidence for the dysconnectivity hypothesis.

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Section: Prefrontal Activation and Cognitive Performancesupporting

confidence: 84%

“…Another meta-analysis demonstrated that this inconsistency primarily depends on task performance (Van Snellenberg et al, 2006). Hence, levels of dlPFC activation may reflect neural processing efficiency indicating individual differences of working memory capacity (Callicott et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Reduced Prefrontal-Parietal Effective Connectivity and Working Memory Deficits in Schizophrenia

et al. 2012

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“…In addition, such deficits in goal maintenance are found in the first-degree relatives of individuals with schizophrenia [56,57], as well as in individuals with schizotypal personality disorder [58,59]. Individuals with schizophrenia also show strong evidence of impairment on other tasks that may tap into goal maintenance, such as the Stroop task [e.g., 60] and the antisaccade task [e.g., 61], as do their first degree relatives [58] Individuals with schizophrenia also show consistent evidence of impaired prefrontal activity, particularly in dorsolateral regions, during tasks that require goal maintenance [e.g., 55,62,63]. Again, the first-degree relatives of individuals with schizophrenia also show evidence of impaired prefrontal activation during goal maintenance [57,64].…”

Section: Strong Evidence Of Impairment In Schizophreniamentioning

confidence: 99%

The Cognitive Neuroscience of Working Memory: Relevance to CNTRICS and Schizophrenia

Deanna

Smith

2008

Biological Psychiatry

156

129

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Working memory is one of the central constructs in cognitive science and has received enormous attention in the theoretical and empirical literature. Similarly, working memory deficits have long been thought to be one of the core cognitive deficits in schizophrenia, making it a ripe area for translation. The current article provides a brief overview of the current theories and data on the psychological and neural mechanisms involved in working memory, which is a summary of the presentation and discussion on working memory that occurred at the first CNTRICS meeting in Washington, D.C. At this meeting, the consensus was that the constructs of goal maintenance and interference control were the most ready to be pursued as part of a translational cognitive neuroscience effort in the remaining CNTRICS meetings. The group felt that the constructs of longterm memory reactivation, capacity, and strategic encoding were of great clinical interest, but required more basic research. In addition, the group felt that the constructs of maintenance over time and updating in working memory had growing construct validity at the psychological and neural levels, but required more research in schizophrenia before knowing whether they should be targets for a clinical trials setting.Working memory is perhaps one of the most frequently studied domains in both cognitive science and cognitive neuroscience, with a wealth of accumulated theoretical and empirical work at both the psychological and neural level [1]. Further, a large body of work has demonstrated that individuals with schizophrenia have deficits on a varied set of working memory tasks [e.g., 2,3] that are associated with impairments in a range of neural mechanisms [4]. There is some data to suggest that the degree of impairment in certain aspects of working memory predicts later onset of schizophrenia [5,6]. In addition, the level of working memory impairment predicts the degree of social and occupational impairment in individuals with schizophrenia [e.g., 7,8]. Further, individuals who share unexpressed genetic components of vulnerability to schizophrenia also experience impairments in working memory function [e.g., 9,10].

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“…Without fully controlling for performance differences over the same dynamic range of WM load, it is difficult to know whether performance deficits in schizophrenia reflect primary dysfunction in task-related networks, suboptimal activation of these networks, and/or downstream effects of other disrupted networks (Van Snellenberg et al, 2006). Indeed, WM function depends not only on activation of dlPFC and other nodes within the frontoparietal control network (FPCN) but also on deactivation of the default mode network (DMN; Anticevic et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Disrupted Working Memory Circuitry in Schizophrenia: Disentangling fMRI Markers of Core Pathology vs Other Aspects of Impaired Performance

Eryilmaz

Tanner

et al. 2016

Neuropsychopharmacol

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Working memory (WM) impairment, a core feature of schizophrenia, is often associated with aberrant dorsolateral prefrontal cortex (dlPFC) activation. Reduced resting-state connectivity within the frontoparietal control network (FPCN) has also been reported in schizophrenia. However, interpretation of WM-related dlPFC dysfunction has been limited by performance differences between patients and controls, and by uncertainty over the relevance of resting-state connectivity to network engagement during task. We contrasted brain activation in 40 schizophrenia patients and 40 controls during verbal WM performance, and evaluated underlying functional connectivity during rest and task. During correct trials, patients demonstrated normal FPCN activation, despite an inverse relationship between positive symptoms and activation. FPCN activation differed between the groups only during error trials (controls4patients). In contrast, controls demonstrated stronger deactivation of the ventromedial prefrontal cortex (vmPFC) during correct and error trials. Functional connectivity analysis indicated impaired resting-state FPCN connectivity in patients, but normal connectivity during task. However, patients showed abnormal connectivity among regions such as vmPFC, lateral orbitofrontal cortex, and parahippocampal gyrus (PHG) during both rest and task. During task, patients also exhibited altered thalamic connectivity to PHG and FPCN. Activation and connectivity patterns that were more characteristic of controls generally correlated with better performance. In summary, patients demonstrated normal FPCN activation when they remained on-task, and exhibited normal FPCN connectivity during WM, whereas vmPFC deactivation differences persisted regardless of WM performance. Our findings suggest that altered FPCN activation in patients reflects performance difference, and that limbic and thalamic dysfunction is critically involved in WM deficits in schizophrenia.

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Functional neuroimaging of working memory in schizophrenia: Task performance as a moderating variable.

Cited by 142 publications

References 59 publications

Reduced Prefrontal-Parietal Effective Connectivity and Working Memory Deficits in Schizophrenia

Reduced Prefrontal-Parietal Effective Connectivity and Working Memory Deficits in Schizophrenia

The Cognitive Neuroscience of Working Memory: Relevance to CNTRICS and Schizophrenia

Disrupted Working Memory Circuitry in Schizophrenia: Disentangling fMRI Markers of Core Pathology vs Other Aspects of Impaired Performance

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