Failure of positive but not negative emotional valence to enhance memory in schizophrenia.

Herbener, Ellen S.; Rosen, Cherise; Khine, Tin; Sweeney, John A.

doi:10.1037/0021-843x.116.1.43

Cited by 100 publications

(94 citation statements)

References 78 publications

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“…Additional exploratory analysis revealed preliminary evidence that ketamine produces a valence-dependent pattern of impairments on longer-term recognition memory performance, with less severe impairments on negative stimuli in the context of intact emotional enhancement for negative information. Two previous studies examining the emotional subsequent memory effect in schizophrenia patients after longer consolidation intervals (< 24h) reported -in addition to generally impaired memory performance in the schizophrenia patients -greater rates of forgetting of both, positive and neutral stimuli than negative stimuli in a sample of long-hospitalized schizophrenia patients (Calev and Edelist, 1993), and a lack of emotional memory enhancement of positive, but intact enhancement of negative stimuli in a sample of stable-medicated schizophrenia patients (Herbener et al, 2007). However, given the preliminary nature of the emotion-specific behavioural effects of ketamine conclusions in this regard need to be drawn with caution.…”

Section: Potential Relevance For Schizophreniamentioning

confidence: 99%

“…A number of studies examined the ESM in schizophrenia patients to specifically probe the disintegration of emotion and cognition (Herbener, 2008). Most ESM studies observed normal emotional experience during encoding in schizophrenia patients (Lakis et al, 2011;Herbener et al, 2007;Hall et al, 2007), however, with regard to the specificity of impairments in the domain of the emotional subsequent memory effect findings remained inconsistent ranging from unspecific impairments (Lakis et al, 2011;Hall et al, 2007) to highly selective impairments for positive information only (Herbener et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, ketamine produced increased activity in the amygdala and orbitofrontal cortex specifically during encoding of negative material. Previous studies on emotional encoding in healthy individuals revealed increased amygdala activity for emotional, particularly negative stimuli (Canli et al, 2000;Fusar-Poli et al, 2009), that has been associated with enhanced long-term recognition memory (Hamann et al, 1999;Herbener et al, 2007). In healthy subjects amygdala reactivity to negative emotional material shows an inverse relationship to prefrontal activity, including the mPFC and superior orbital regions, thought to reflect prefrontal top-down emotion regulation of the amygdala (Buhl et al, 2014;Etkin et al, 2011, Kober et al, 2008Diekhof et al, 2011), suggesting that the interaction of valence-independent suppression of mPFC regulatory functioning during ketamine with valence-dependent amygdala reactivity, i.e.…”

Section: Valence-specific Effects Of Ketaminementioning

confidence: 99%

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General and emotion-specific neural effects of ketamine during emotional memory formation

et al. 2017

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General and emotion-specific neural effects of ketamine during emotional memory formation, NeuroImage, http://dx.doi.org/10. 1016/j.neuroimage.2017.02.049 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractAnimal studies suggest that N-methyl-D-aspartate receptor (NMDAR) dependent signalling in limbic and prefrontal regions is critically involved in both cognitive and emotional functions. In humans, ketamine-induced transient, and disorder associated chronic NMDAR hypofunction (i.e. in schizophrenia) has been associated with deficient performance in the domains of memory and higher-order emotional functioning, as well as altered neural activity in the underlying limbicprefrontal circuits. To model the effects of NMDAR hypofunction on the integration of emotion and cognition the present pharmacological fMRI study applied the NMDAR antagonist ketamine (target plasma level = 100ng/ml) to 21 healthy volunteers in a within-subject placebo-controlled crossover 2 design during encoding of neutral, positive and negative pictures. Our results show that irrespective of emotion, ketamine suppressed parahippocampal and medial prefrontal activity. In contrast, ketamine selectively increased amygdala and orbitofrontal activity during successful encoding of negative stimuli. On the network level ketamine generally increased medial prefrontalparahippocampal coupling while specifically decreasing amygdala-orbitofrontal interplay during encoding of negative stimuli. On the behavioural level, ketamine produced generally decreased memory performance and abolished the emotional enhancement of memory after a wash-out period of 5 days. The present findings suggest that ketamine produces general as well as valencespecific effects during emotional memory formation. The pattern partly overlaps with alterations previously observed in patients with schizophrenia.

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Section: Potential Relevance For Schizophreniamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Valence-specific Effects Of Ketaminementioning

confidence: 99%

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General and emotion-specific neural effects of ketamine during emotional memory formation

et al. 2017

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“…222,223 However, symptoms such as anhedonia and avolition also represent significant constraints on functional outcome in this illness. The presence of anhedonia is associated with poor community and social function 99,[224][225][226][227][228] and predicts poor longterm outcomes. 99,[229][230][231] It may turn out that some of the same mechanisms leading to cognitive deficits in schizophrenia also contribute to anhedonia and avolition, such as DLPFC-mediated disturbances in goal maintenance.…”

Section: Summary Suggestions For Future Research and Significancementioning

confidence: 99%

“…The presence of anhedonia is associated with poor community and social function 99,[224][225][226][227][228] and predicts poor longterm outcomes. 99,[229][230][231] It may turn out that some of the same mechanisms leading to cognitive deficits in schizophrenia also contribute to anhedonia and avolition, such as DLPFC-mediated disturbances in goal maintenance. 232,233 If so, then treatments aimed at improving cognitive function in schizophrenia may also improve anhedonia and avolition, though there is not yet clear evidence for this.…”

Section: Summary Suggestions For Future Research and Significancementioning

confidence: 99%

Goal Representations and Motivational Drive in Schizophrenia: The Role of Prefrontal-Striatal Interactions

Deanna

Dowd

2010

Schizophrenia Bulletin

428

325

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The past several years have seen a resurgence of interest in understanding the psychological and neural bases of what are often referred to as ''negative symptoms'' in schizophrenia. These aspects of schizophrenia include constructs such as asociality, avolition (a reduction in the motivation to initiate or persist in goal-directed behavior), and anhedonia (a reduction in the ability to experience pleasure). We believe that these dimensions of impairment in individuals with schizophrenia reflect difficulties using internal representations of emotional experiences, previous rewards, and motivational goals to drive current and future behavior in a way that would allow them to obtain desired outcomes, a deficit that has major clinical significance in terms of functional capacity. In this article, we review the major components of the systems that link experienced and anticipated rewards with motivated behavior that could potentially be impaired in schizophrenia. We conclude that the existing evidence suggests relatively intact hedonics in schizophrenia, but impairments in some aspects of reinforcement learning, reward prediction, and prediction error processing, consistent with an impairment in ''wanting.'' As of yet, there is only indirect evidence of impairment in anterior cingulate and orbital frontal function that may support value and effort computations. However, there are intriguing hints that individuals with schizophrenia may not be able to use reward information to modulate cognitive control and dorsolateral prefrontal cortex function, suggesting a potentially important role for cortical-striatal interactions in mediating impairment in motivated and goal-directed behavior in schizophrenia.

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Mechanisms Underlying Motivational Deficits in Psychopathology: Similarities and Differences in Depression and Schizophrenia

Deanna¹,

Pagliaccio²,

Luking³

2015

Current Topics in Behavioral Neurosciences

191

151

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Motivational and hedonic impairments are core aspects of a variety of types of psychopathology. These impairments cut across diagnostic categories and may be critical to understanding major aspects of the functional impairments accompanying psychopathology. Given the centrality of motivational and hedonic systems to psychopathology, the Research Domain Criteria (RDoC) initiative includes a "positive valence" systems domain that outlines a number of constructs that may be key to understanding the nature and mechanisms of motivational and hedonic impairments in psychopathology. These component constructs include initial responsiveness to reward, reward anticipation or expectancy, incentive or reinforcement learning, effort valuation, and action selection. Here, we review behavioral and neuroimaging studies providing evidence for impairments in these constructs in individuals with psychosis versus in individuals with depressive pathology. There are important differences in the nature of reward-related and hedonic deficits associated with psychosis versus depression that have major implications for our understanding of etiology and treatment development. In particular, the literature strongly suggests the presence of impairments in in-the-moment hedonics or "liking" in individuals with depressive pathology, particularly among those who experience anhedonia. Such deficits may propagate forward and contribute to impairments in other constructs that are dependent on hedonic responses, such as anticipation, learning, effort, and action selection. Such hedonic impairments could reflect alterations in dopamine and/or opioid signaling in the striatum related to depression or specifically to anhedonia in depressed populations. In contrast, the literature points to relatively intact in-the-moment hedonic processing in psychosis, but provides much evidence for impairments in other components involved in translating reward to action selection. Particularly, individuals with schizophrenia exhibit altered reward prediction and associated striatal and prefrontal activation, impaired reward learning, and impaired reward-modulated action selection.

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Failure of positive but not negative emotional valence to enhance memory in schizophrenia.

Cited by 100 publications

References 78 publications

General and emotion-specific neural effects of ketamine during emotional memory formation

General and emotion-specific neural effects of ketamine during emotional memory formation

Goal Representations and Motivational Drive in Schizophrenia: The Role of Prefrontal-Striatal Interactions

Mechanisms Underlying Motivational Deficits in Psychopathology: Similarities and Differences in Depression and Schizophrenia

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