Altered representation of expected value in the orbitofrontal cortex in mania

Bermpohl, Felix; Kahnt, Thorsten; Dalanay, Umut; Hägele, Claudia; Sajonz, Bastian; Wegner, Tristan; Stoy, Meline; Adli, Mazda; Krüger, Stephanie; Wrase, Jana; Ströhle, Andreas; Bauer, Michael; Heinz, Andreas

doi:10.1002/hbm.20909

Cited by 127 publications

(110 citation statements)

References 65 publications

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“…Manic behavior consists in part of impairment in these domains, with patients displaying exaggerated reward-seeking behaviors and overoptimistically assessing the outcomes of their actions. It is unclear what relative roles the NA, striatum and orbitofrontal cortex (OFC) might play in mania: stimulation at the NA has been observed to produce euphoria [31] , the striatum has been tied to the experience of pleasure [29] and fMRI data suggest that OFC abnormalities can be present in patients with mania during expected-gain tasks [32] . There is some evidence that ALIC-NA DBS modulates these circuits: high-frequency stimulation of the NA has been shown to inhibit the firing of OFC neurons in rats [33] and intraoperative ventral ALIC-NA stimulation has been found to acutely elevate mood [31] .…”

Section: Discussionmentioning

confidence: 99%

A Case of Mania following Deep Brain Stimulation for Obsessive Compulsive Disorder

Haq

Foote

Goodman

et al. 2010

Stereotact Funct Neurosurg

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Deep brain stimulation (DBS) of the basal ganglia is an effective treatment for select movement disorders, including Parkinson’s disease, essential tremor and dystonia. Based on these successes, DBS has been explored as an experimental treatment for medication-resistant neuropsychiatric disease. During a multiyear experience employing DBS to treat patients for obsessive compulsive disorder (OCD) we encountered several unanticipated stimulation-induced psychiatric side effects. We present a case of a young woman treated for OCD with DBS of the anterior limb of the internal capsule and nucleus accumbens region, who subsequently manifested a manic episode. We aim to discuss the case details, treatment and potential neuroanatomical underpinnings of this response.

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Section: Discussionmentioning

confidence: 99%

A Case of Mania following Deep Brain Stimulation for Obsessive Compulsive Disorder

Haq

Foote

Goodman

et al. 2010

Stereotact Funct Neurosurg

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“…2a .) This type of non-reward or punishment-related responsiveness has been found to be very different in mania, with apparently decreasing activations in the lateral orbitofrontal cortex during expectation of increasing loss (Bermpohl et al, 2010), the opposite of what is found in healthy participants (Grabenhorst and Rolls, 2011;O'Doherty et al, 2001). In this context, of potentially reduced sensitivity or even abnormal function of the lateral orbitofrontal cortex non-reward system in mania, it is relevant that manic bipolar patients continue to pursue immediate rewards despite negative consequences (Wessa et al, 2014).…”

Section: Mania and Bipolar Disordermentioning

confidence: 99%

A non-reward attractor theory of depression

Rolls

2016

Neuroscience & Biobehavioral Reviews

153

174

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Neuroscience and Biobehavioral Reviews, in press (May 2016) \papers\Emotion\depression\depression16b.docx 2 SummaryA non-reward attractor theory of depression is proposed based on the operation of the lateral orbitofrontal cortex and supracallosal cingulate cortex. The orbitofrontal cortex contains error neurons that respond to non-reward for many seconds in an attractor state that maintains a memory of the nonreward. The human lateral orbitofrontal cortex is activated by non-reward during reward reversal, and by a signal to stop a response that is now incorrect. Damage to the human orbitofrontal cortex impairs reward reversal learning. Not receiving reward can produce depression. The theory proposed is that in depression, this lateral orbitofrontal cortex non-reward system is more easily triggered, and maintains its attractor-related firing for longer. This triggers negative cognitive states, which in turn have positive feedback top-down effects on the orbitofrontal cortex non-reward system. Treatments for depression, including ketamine, may act in part by quashing this attractor. The mania of bipolar disorder is hypothesized to be associated with oversensitivity and overactivity in the reciprocally related reward system in the medial orbitofrontal cortex and pregenual cingulate cortex.

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“…It is likely that our sample size (n ¼ 20 per group) was insufficiently powered to detect diagnostic effects during these phases using this type of multi-level model. Therefore, future studies comparing cases and controls using larger sample sizes and/or tasks with more trials per event type to assess magnitude-related factors such as expected value encoding are needed to assess these factors in unmedicated BD (Bermpohl et al, 2010).…”

Section: Whole-brain Findingsmentioning

confidence: 99%

Hypoactivation of the Ventral and Dorsal Striatum During Reward and Loss Anticipation in Antipsychotic and Mood Stabilizer-Naive Bipolar Disorder

Yip

Worhunsky

Rogers

et al. 2014

Neuropsychopharmacol

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Increased activity within known reward-processing neurocircuitry (eg, ventral striatum, VS) has been reported among medicated individuals with bipolar disorder (BD) I and II. However, such findings are confounded by the potential ameliorative effects of moodstabilizing and antipsychotic medications on neural activations. This study tests the hypothesis that a pathophysiological locus of alterations in reward processing is present within the striatum in antipsychotic and lithium-naive individuals with BD. Twenty antipsychotic and lithium-naive individuals with BD II or BD not-otherwise specified (NOS) and 20 matched healthy comparison individuals participated in functional magnetic resonance imaging during the performance of a monetary incentive delay task. Between-group comparisons were conducted using small-volume correction focusing on orthogonal a priori regions of interest centered in the VS and dorsal striatum (DS), respectively. During reward anticipation, unmedicated individuals with BD II/NOS had decreased activity within the DS (but not VS). During loss anticipation, on the other hand, decreased activation within both the VS and DS was observed. Across all participants, DS activity (during reward anticipation) was positively associated with putamen volume. This is the first report of decreased dorsal and ventral striatal activity among unmedicated individuals with BD II/NOS. These data contradict a simple 'reward hypersensitivity' model of BD, and add to a growing body of literature suggesting that blunted reward processing may be a vulnerability factor for both mood-and addiction-related disorders.

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Altered representation of expected value in the orbitofrontal cortex in mania

Cited by 127 publications

References 65 publications

A Case of Mania following Deep Brain Stimulation for Obsessive Compulsive Disorder

A Case of Mania following Deep Brain Stimulation for Obsessive Compulsive Disorder

A non-reward attractor theory of depression

Hypoactivation of the Ventral and Dorsal Striatum During Reward and Loss Anticipation in Antipsychotic and Mood Stabilizer-Naive Bipolar Disorder

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