Search

Rumination is a process of uncontrolled, narrowly focused negative thinking that is often self-referential, and that is a hallmark of depression. Despite its importance, little is known about its cognitive mechanisms. Rumination can be thought of as a specific, constrained form of mind-wandering. Here, we introduce a cognitive model of rumination that we developed on the basis of our existing model of mind-wandering. The rumination model implements the hypothesis that rumination is caused by maladaptive habits of thought. These habits of thought are modeled by adjusting the number of memory chunks and their associative structure, which changes the sequence of memories that are retrieved during mind-wandering, such that during rumination the same set of negative memories is retrieved repeatedly. The implementation of habits of thought was guided by empirical data from an experience sampling study in healthy and depressed participants. On the basis of this empirically derived memory structure, our model naturally predicts the declines in cognitive task performance that are typically observed in depressed patients. This study demonstrates how we can use cognitive models to better understand the cognitive mechanisms underlying rumination and depression.Van Vugt, van der Velde, and collaborators show how cognitive architectures can implement verbal theories of psychiatric problems. They show how one theory of depressive rumination can be implemented in the ACT-R cognitive architecture by changing the contents of its simulated memory. These manipulations of memory habits lead the model to show impairments in a sustained attention task--a plausible impairment given that people who suffer from depression have concentration complaints.

cite as: Lataster, J., Collip, D., Ceccarini, J., Haas, D., Booij, L., van Os, J., Pruessner, J., Van Laere, K., & Myin-Germeys, I. (2011). Psychosocial stress is associated with in vivo dopamine release in human ventromedial prefrontal cortex: a positron emission tomography study using [18F] fallypride. Neuroimage, 58(4), 1081-1089.DOI: 10.1016/j.neuroimage.2011.07.030AbstractRodent studies suggest that prefrontal dopamine neurotransmission plays an important role in the neural processing of psychosocial stress. Human studies investigating stress-induced changes in dopamine levels, however, have focused solely on striatal dopamine transmission. The aim of this study was to investigate in vivo dopamine release in the human prefrontal cortex in response to a psychosocial stress challenge, using the highly selective dopamine D2/3 PET radioligand [18F]fallypride in healthy subjects. Twelve healthy subjects (age (y): 39.8; SD = 15.8) underwenta single dynamic Positron Emission Tomography (PET) scanning session after intravenous administration of 185.2 (SD = 10.2) MBq [18F]fallypride. Psychosocial stress was initiated at 100minutes postinjection. PET data were analyzed using the linearized simplified reference region model (LSRRM), which accounts for time-dependent changes in [18F]fallypride displacement.Voxel-based statistical maps, representing specific D2/3 binding changes, were computed to localize areas with increased ligand displacement after task initiation, reflecting dopamine release. The psychosocial stress challenge induced detectable amounts of dopamine release throughout the prefrontal cortex, with dopaminergic activity in bilateral ventromedial prefrontal cortex being associated with subjectively rated experiences of psychosocial stress. The novel finding that a mild psychosocial stress in humans induces increased levels of endogenous dopamine in the PFC indicates that the dynamics of the dopamine-related stress response cannot be interpreted by focusing on mesolimbic brain regions alone.

see alsoLataster, J., Collip, D., Ceccarini, J., Haas, D., Booij, L., van Os, J., ... & Myin-Germeys, I. (2011). Psychosocial stress is associated with in vivo dopamine release in human ventromedial prefrontal cortex: a positron emission tomography study using [18F] fallypride. Neuroimage, 58(4), 1081-1089.DOI: 10.1016/j.neuroimage.2011.07.030Rodent studies suggest that prefrontal dopamine neurotransmission plays an important role in the neural processing of psychosocial stress. Human studies investigating stress-induced changes in dopamine levels, however, have focused solely on striatal dopamine transmission. The aim of this study was to investigate in vivo dopamine release in the human prefrontal cortex in response to a psychosocial stress challenge, using the highly selective dopamine D₂/₃ PET radioligand [¹⁸F]fallypride in healthy subjects. Twelve healthy subjects (age (y): 39.8; SD=15.8) underwent a single dynamic Positron Emission Tomography (PET) scanning session after intravenous administration of 185.2 (SD=10.2) MBq [¹⁸F]fallypride. Psychosocial stress was initiated at 100 min postinjection. PET data were analyzed using the linearized simplified reference region model (LSRRM), which accounts for time-dependent changes in [¹⁸F]fallypride displacement. Voxel-based statistical maps, representing specific D₂/₃ binding changes, were computed to localize areas with increased ligand displacement after task initiation, reflecting dopamine release. The psychosocial stress challenge induced detectable amounts of dopamine release throughout the prefrontal cortex, with dopaminergic activity in bilateral ventromedial prefrontal cortex being associated with subjectively rated experiences of psychosocial stress. The novel finding that a mild psychosocial stress in humans induces increased levels of endogenous dopamine in the PFC indicates that the dynamics of the dopamine-related stress response cannot be interpreted by focusing on mesolimbic brain regions alone.

BackgroundPsychotic reactivity to stress has been shown to be dependent from an interaction between (i) genetically and environmentally predisposed vulnerabilities, and (ii) the impact of environmental changes experienced as stressful. The underlying biological mechanisms and the origins of this sensitization to stress, resulting in psychotic experiences, are however unknown.Promising neurobiological candidates that may mediate psychotic reactivity to stress are an abnormal hypothalamic-pituitary-adrenal (HPA) axis reactivity as well as dysfunctional dopamine reactivity. Possible origins of psychotic reactivity to stress are expected to be related to genetic polymorphisms associated with psychosis, stress-reactivity, and HPA-axis functioning. In the current study we will be investigating the phenomenology, underlying biological mechanisms, and related genetic polymorphisms of psychotic reactivity to stress.MethodsTo cover different intensities of the psychotic spectrum, three groups, including unmedicated psychotic patients, first-degree relatives of patients and subjects psychometrically at risk for psychosis, will be compared to healthy control subjects with no history of psychosis.A repeated momentary self-assessment technique (Experience Sampling Method; ESM) in combination with an experimental psychosocial stress task will be used to evaluate psychotic reactivity to stress.Positron Emission Tomography (PET) will be utilized as an imaging tool to assess dopaminergic neurotransmission in response to experimentally induced psychosocial stress. In addition, cortisol measurements, as an indicator of HPA-axis functioning, will be monitored during experimental and daily life stressors. Finally, gene polymorphism data are collected through saliva sampling.HypothesesWe hypothesize that (i) the level of psychotic reactivity is different between subject-groups, (ii) psychotic reactivity is mediated by biological reactivity (cortisol, dopamine) and will differ between groups, (iii) the level of psychotic reactivity is influenced by genetic polymorphisms and early trauma and will differ between groups.see also:Lataster, J., Myin‐Germeys, I., Lieb, R., Wittchen, H. U., & van Os, J. (2012). Adversity and psychosis: a 10‐year prospective study investigating synergism between early and recent adversity in psychosis. Acta psychiatrica scandinavica, 125(5), 388-399.DOI: 10.1111/j.1600-0447.2011.01805.xLataster, J., Collip, D., Ceccarini, J., Hernaus, D., Haas, D., Booij, L., ... & Myin-Germeys, I. (2013). Familial liability to psychosis is associated with attenuated dopamine stress signaling in ventromedial prefrontal cortex. Schizophrenia bulletin, 40(1), 66-77.DOI: 10.1093/schbul/sbs187Lataster, J., Collip, D., Ceccarini, J., Haas, D., Booij, L., van Os, J., ... & Myin-Germeys, I. (2011). Psychosocial stress is associated with in vivo dopamine release in human ventromedial prefrontal cortex: a positron emission tomography study using [18 F] fallypride. Neuroimage, 58(4), 1081-1089.DOI: 10.1016/j.neuroimage.2011.07.030Collip, D., Nicolson, N. A., Lardinois, M., Lataster, T., Van Os, J., & Myin-Germeys, I. (2011). Daily cortisol, stress reactivity and psychotic experiences in individuals at above average genetic risk for psychosis. Psychological medicine, 41(11), 2305-2315.Collip, D., Myin-Germeys, I., Wichers, M., Jacobs, N., Derom, C., Thiery, E., ... & Van Os, J. (2013). FKBP5 as a possible moderator of the psychosis-inducing effects of childhood trauma. The British Journal of Psychiatry, 202(4), 261-268.Collip, D., van Winkel, R., Peerbooms, O., Lataster, T., Thewissen, V., Lardinois, M., ... & Myin‐Germeys, I. (2011). COMT Val158Met–stress interaction in psychosis: role of background psychosis risk. CNS neuroscience & therapeutics, 17(6), 612-619.Collip, D., Myin-Germeys, I., & Van Os, J. (2008). Does the concept of “sensitization” provide a plausible mechanism for the putative link between the environment and schizophrenia?. Schizophrenia bulletin, 34(2), 220-225.

Patients diagnosed with a psychotic disorder and their first-degree relatives display increased reactivity to stress. Although experience of psychosocial stress is associated both with ventromedial prefrontal and mesolimbic dopamine neurotransmission, the role of prefrontal dopamine transmission in the stress psychosis phenotype remains underresearched. The current study aimed at investigating stress-induced in vivo dopamine release in ventromedial prefrontal cortex (vmPFC) of individuals at familial risk for psychosis. first-degree relatives of patients with a psychotic disorder displayed attenuated dopamine stress neuromodulation in vmpfC, possibly reflecting reduced prefrontal regulation of stress-induced mesolimbic dopamine release.see alsoLataster, J., Collip, D., Ceccarini, J., Hernaus, D., Haas, D., Booij, L., ... & Myin-Germeys, I. (2013). Familial liability to psychosis is associated with attenuated dopamine stress signaling in ventromedial prefrontal cortex. Schizophrenia bulletin, 40(1), 66-77.DOI: 10.1093/schbul/sbs187

BackgroundPsychotic reactivity to stress has been shown to be dependent from an interaction between (i) genetically and environmentally predisposed vulnerabilities, and (ii) the impact of environmental changes experienced as stressful. The underlying biological mechanisms and the origins of this sensitization to stress, resulting in psychotic experiences, are however unknown.Promising neurobiological candidates that may mediate psychotic reactivity to stress are an abnormal hypothalamic-pituitary-adrenal (HPA) axis reactivity as well as dysfunctional dopamine reactivity. Possible origins of psychotic reactivity to stress are expected to be related to genetic polymorphisms associated with psychosis, stress-reactivity, and HPA-axis functioning. In the current study we will be investigating the phenomenology, underlying biological mechanisms, and related genetic polymorphisms of psychotic reactivity to stress.MethodsTo cover different intensities of the psychotic spectrum, three groups, including unmedicated psychotic patients, first-degree relatives of patients and subjects psychometrically at risk for psychosis, will be compared to healthy control subjects with no history of psychosis.A repeated momentary self-assessment technique (Experience Sampling Method; ESM) in combination with an experimental psychosocial stress task will be used to evaluate psychotic reactivity to stress.Positron Emission Tomography (PET) will be utilized as an imaging tool to assess dopaminergic neurotransmission in response to experimentally induced psychosocial stress. In addition, cortisol measurements, as an indicator of HPA-axis functioning, will be monitored during experimental and daily life stressors. Finally, gene polymorphism data are collected through saliva sampling.HypothesesWe hypothesize that (i) the level of psychotic reactivity is different between subject-groups, (ii) psychotic reactivity is mediated by biological reactivity (cortisol, dopamine) and will differ between groups, (iii) the level of psychotic reactivity is influenced by genetic polymorphisms and early trauma and will differ between groups.

Patients diagnosed with a psychotic disorder and their first-degree relatives display increased reactivity to stress. Although experience of psychosocial stress is associated both with ventromedial prefrontal and mesolimbic dopamine neurotransmission, the role of prefrontal dopamine transmission in the stress psychosis phenotype remains underresearched. The current study aimed at investigating stress-induced in vivo dopamine release in ventromedial prefrontal cortex (vmPFC) of individuals at familial risk for psychosis. first-degree relatives of patients with a psychotic disorder displayed attenuated dopamine stress neuromodulation in vmpfC, possibly reflecting reduced prefrontal regulation of stress-induced mesolimbic dopamine release.see also:Lataster, J., Collip, D., Ceccarini, J., Hernaus, D., Haas, D., Booij, L., ... & Myin-Germeys, I. (2013). Familial liability to psychosis is associated with attenuated dopamine stress signaling in ventromedial prefrontal cortex. Schizophrenia bulletin, 40(1), 66-77.

Objective: Patients diagnosed with a psychotic disorder and their first-degree relatives display increased reactivity to stress. Theory predicts that experience of psychosocial stress is associated both with ventromedial prefrontal and mesolimbic dopamine neurotransmission. However, while there is evidence of aberrant striatal dopamine processing in psychotic disorder, the role of the prefrontal cortex remains under-researched. This study aimed at investigating stress-induced in vivo dopamine release in ventromedial prefrontal cortex (vmPFC) of individuals at familial risk for psychosis. Method: Fourteen healthy first-degree relatives of patients with a diagnosis of psychotic disorder and 10 control subjects underwent a single dynamic positron emission tomography (PET) scanning session after intravenous administration of 183.2 (SD = 7.6) MBq [18F]fallypride. Psychosocial stress was initiated at 100min postinjection using a computerized mental arithmetic task with social evaluative threat components. PET data were analyzed using the linearized simplified reference region model. Regression analyses were performed to compare the spatial extent of task-related ligand displacement between control subjects and relatives and to find how it related to self-rated experiences of psychosocial stress and psychosis. Results: First-degree relatives displayed hyporeactive dopamine signaling in the vmPFC in response to stress. Increased levels of subjectively rated stress were associated with increased intensity of psychotic experiences. This effect was particularly pronounced in first-degree relatives. Conclusion: Although previous studies have hypothesized a role for prefrontal dopamine dysfunction in psychosis, this study, to our knowledge, is the first in vivo human imaging study showing attenuated (ie, hyporeactive) dopamine stress neuromodulation in vmPFC of individuals at familial risk for psychosis.see also:Lataster, J., Collip, D., Ceccarini, J., Hernaus, D., Haas, D., Booij, L., ... & Myin-Germeys, I. (2013). Familial liability to psychosis is associated with attenuated dopamine stress signaling in ventromedial prefrontal cortex. Schizophrenia bulletin, 40(1), 66-77.DOI: 10.1093/schbul/sbs187

Rodent studies suggest that prefrontal dopamine neurotransmission plays an important role in the neural processing of psychosocial stress. Human studies investigating stress-induced changes in dopamine levels, however, have focused solely on striatal dopamine transmission. The aim of this study was to investigate in vivo dopamine release in the human prefrontal cortex in response to a psychosocial stress challenge, using the highly selective dopamine D2/3 PET radioligand [18F]fallypride in healthy subjects. Twelve healthy subjects (age (y): 39.8; SD = 15.8) underwent a single dynamic Positron Emission Tomography (PET) scanning session after intravenous administration of 185.2 (SD = 10.2) MBq [18F]fallypride. Psychosocial stress was initiated at 100 min postinjection. PET data were analyzed using the linearized simplified reference region model (LSRRM), which accounts for time-dependent changes in [18F]fallypride displacement. Voxel-based statistical maps, representing specific D2/3 binding changes, were computed to localize areas with increased ligand displacement after task initiation, reflecting dopamine release. The psychosocial stress challenge induced detectable amounts of dopamine release throughout the prefrontal cortex, with dopaminergic activity in bilateral ventromedial prefrontal cortex being associated with subjectively rated experiences of psychosocial stress. The novel finding that a mild psychosocial stress in humans induces increased levels of endogenous dopamine in the PFC indicates that the dynamics of the dopamine-related stress response cannot be interpreted by focusing on mesolimbic brain regions alone.see also:Lataster, J., Collip, D., Ceccarini, J., Haas, D., Booij, L., van Os, J., ... & Myin-Germeys, I. (2011). Psychosocial stress is associated with in vivo dopamine release in human ventromedial prefrontal cortex: a positron emission tomography study using [18 F] fallypride. Neuroimage, 58(4), 1081-1089.DOI: 10.1016/j.neuroimage.2011.07.030

BackgroundPsychotic reactivity to stress has been shown to be dependent from an interaction between (i) genetically and environmentally predisposed vulnerabilities, and (ii) the impact of environmental changes experienced as stressful. The underlying biological mechanisms and the origins of this sensitization to stress, resulting in psychotic experiences, are however unknown.Promising neurobiological candidates that may mediate psychotic reactivity to stress are an abnormal hypothalamic-pituitary-adrenal (HPA) axis reactivity as well as dysfunctional dopamine reactivity. Possible origins of psychotic reactivity to stress are expected to be related to genetic polymorphisms associated with psychosis, stress-reactivity, and HPA-axis functioning. In the current study we will be investigating the phenomenology, underlying biological mechanisms, and related genetic polymorphisms of psychotic reactivity to stress.MethodsTo cover different intensities of the psychotic spectrum, three groups, including unmedicated psychotic patients, first-degree relatives of patients and subjects psychometrically at risk for psychosis, will be compared to healthy control subjects with no history of psychosis.A repeated momentary self-assessment technique (Experience Sampling Method; ESM) in combination with an experimental psychosocial stress task will be used to evaluate psychotic reactivity to stress.Positron Emission Tomography (PET) will be utilized as an imaging tool to assess dopaminergic neurotransmission in response to experimentally induced psychosocial stress. In addition, cortisol measurements, as an indicator of HPA-axis functioning, will be monitored during experimental and daily life stressors. Finally, gene polymorphism data are collected through saliva sampling.HypothesesWe hypothesize that (i) the level of psychotic reactivity is different between subject-groups, (ii) psychotic reactivity is mediated by biological reactivity (cortisol, dopamine) and will differ between groups, (iii) the level of psychotic reactivity is influenced by genetic polymorphisms and early trauma and will differ between groups.see also:Lataster, J., Myin‐Germeys, I., Lieb, R., Wittchen, H. U., & van Os, J. (2012). Adversity and psychosis: a 10‐year prospective study investigating synergism between early and recent adversity in psychosis. Acta psychiatrica scandinavica, 125(5), 388-399.Lataster, J., Collip, D., Ceccarini, J., Hernaus, D., Haas, D., Booij, L., ... & Myin-Germeys, I. (2013). Familial liability to psychosis is associated with attenuated dopamine stress signaling in ventromedial prefrontal cortex. Schizophrenia bulletin, 40(1), 66-77.Lataster, J., Collip, D., Ceccarini, J., Haas, D., Booij, L., van Os, J., ... & Myin-Germeys, I. (2011). Psychosocial stress is associated with in vivo dopamine release in human ventromedial prefrontal cortex: a positron emission tomography study using [18 F] fallypride. Neuroimage, 58(4), 1081-1089.Collip, D., Nicolson, N. A., Lardinois, M., Lataster, T., Van Os, J., & Myin-Germeys, I. (2011). Daily cortisol, stress reactivity and psychotic experiences in individuals at above average genetic risk for psychosis. Psychological medicine, 41(11), 2305-2315.Collip, D., Myin-Germeys, I., Wichers, M., Jacobs, N., Derom, C., Thiery, E., ... & Van Os, J. (2013). FKBP5 as a possible moderator of the psychosis-inducing effects of childhood trauma. The British Journal of Psychiatry, 202(4), 261-268.Collip, D., van Winkel, R., Peerbooms, O., Lataster, T., Thewissen, V., Lardinois, M., ... & Myin‐Germeys, I. (2011). COMT Val158Met–stress interaction in psychosis: role of background psychosis risk. CNS neuroscience & therapeutics, 17(6), 612-619.Collip, D., Myin-Germeys, I., & Van Os, J. (2008). Does the concept of “sensitization” provide a plausible mechanism for the putative link between the environment and schizophrenia?. Schizophrenia bulletin, 34(2), 220-225.